ACTIVATION OF T LYMPHOCYTES AND CELL MEDIATED IMMUNITY

Size: px
Start display at page:

Download "ACTIVATION OF T LYMPHOCYTES AND CELL MEDIATED IMMUNITY"

Transcription

1 ACTIVATION OF T LYMPHOCYTES AND CELL MEDIATED IMMUNITY The recognition of specific antigen by naïve T cell induces its own activation and effector phases. T helper cells recognize peptide antigens through its TCR when the antigen is presented to it by an antigen presenting cell along with self-mhc II molecules. This stimulation is strengthened by binding of CD4 molecule of T cell to β2 chain of MHC II protein. Cytotoxic T cells recognize peptide antigen when presented to it with MHC class I proteins. The CD8 molecule of cytotoxic cell binds to α3 domain of class I molecule. The primary stimulation is further enhanced by binding of other accessory molecules; these include CD28 of T cells to B7 of APCs, LFA-1 of T cells to ICAM-1 of APCs, and CD2 of T cells and LFA-3 of APCs. Antigen recognition by effector T cells triggers the effector functions that eliminate the antigen. The outcome of T cell antigen recognition is determined by the duration and affinity of the TCR-antigen interaction. On any APC, approximately only 1000 out of ~10 5 available MHC molecules are likely to display any one peptide at any time. Incomplete signaling may not lead to any response; insufficient signaling may even inactivate the T cell. Dendritic cells and macrophages are efficient APCs because they express high number of MHC molecules and co-receptors than other APCs. Memory and effector T cells have less threshold for activation than naïve T cells and can respond to antigens that are presented by other APCs. Memory and effector T cells can be stimulated in peripheral tissues outside the secondary lymphoid organs. This allows quick response by T cells wherever they encounter the same antigen. If a recently activated T cell is repeatedly exposed to same antigen, some T cells undergo apoptosis. This is called activation-induced cell death and plays a role in self-tolerance. In the absence of co-stimulation, T cells either fail to respond and die by apoptosis or enter a state of unresponsiveness called anergy. Binding of CD28 to B7-1 or B7-2 on APCs delivers signals that enhance T cell response to antigen, prolong cell survival, production of cytokine (IL-2) and differentiation of naïve cells to effector cells. On APCs other than macrophages and dendritic cells, B7 molecules are expressed at low levels but can be induced to increase expression by bacterial endotoxins, IFN-γ, and binding of T cell CD40L to CD40 on APCs. Adjuvants are also known to induce expression of co-stimulators. APCs in normal tissues contribute to maintenance of tolerance to self-antigens. This is because even though such cells are able to process and present self antigens, lack of co-stimulation results in no activation of T cells. In addition to CD28, other T cell receptors like CD2 can deliver co-stimulatory signals. CD-2 binds to its ligand LFA-3 on APC and delivers costimulatory signals even in the absence of CD28. The interaction of CD40L on T cell with CD40 on APC enhances T cell activation by inducing the expression of B7 molecule on APC and inducing the APC to secrete cytokines such as IL-12 that act on T cells. IL-12 provides necessary signal for T cell proliferation.

2 CD28-B7 interactions and CD2-LFA-3 interactions promote T cell activation by enhancing transcription in T cell, increase the production of cytokine (IL-2), and promote T cell survival. The recognition of antigen initiates a sequence of biochemical signals in T cells that result in activation of certain genes and the entry of cell into cell cycle. The genes that are activated are responsible for production of proteins that mediate effector functions. The cellular response of T cells to antigens consists of three stages: 1. membrane events, which occur within seconds 2. cytoplasmic signal transduction pathways, which occur within minutes 3. new gene transcription, which occur within hours One of the first steps in activation of T cells is the production of IL-2 by the antigen-stimulated T cell. IL-2 functions as growth and differentiation factor for T cells. On stimulation, T cells also increase the expression of receptors for many cytokines. One such activation receptor that is produced by T cell is IL-2 receptor. The activated T cells secrete IL-2, which act on themselves; hence IL-2 is considered an autocrine growth factor. This results in clonal proliferation of the activated T cells. The progeny of antigen-stimulated CD4+ T cells differentiate into effector T cells that produce cytokines. Subsets of effector CD4+ T cells, namely Th1 and Th2, secrete different cytokines and perform different functions. CD8+ T cells differentiate into functional cytotoxic T cells. The differentiation of T cells is associated with production of effector molecules such as cytokines, cytotoxic granule proteins and ligands such as CD40 Fas protein. The major effector function of CD4+ T helper cells is to activate macrophage and other lymphocytes (e.g., B cell) by the production of cytokines whereas the major effector function of CD8+ T cells is to lyse the antigen bearing target cells. The cytokines produced by helper T cells act on themselves, other T cells, B cells, macrophages, granulocytes and vascular endothelium. Thus these cytokines participate in cell mediated 2

3 immunity, humoral immunity as well as inflammation. Macrophages and B lymphocytes that present antigens to T helper cells, get activated by the same T cell. Cell mediated immunity (CMI) is the effector function of T lymphocytes. CMI can be transferred to another individual passively by transfer of viable T lymphocytes, this is termed adoptive immunity. It is the principal mechanism of defense against those pathogens that survive within macrophages or infect non-phagocytic cells. Defect in CMI leads to increased susceptibility to virus and intracellular bacteria. T cells that are responsible for activation of macrophage are the differentiated Th1 subsets of CD4+ T cells as well as CD8+ T cells, since both these cells are capable of secreting macrophage activating cytokine, IFN-γ. CMI is responsible for rejection of grafts containing cells that exhibit non-self MHC proteins as well as elimination of cells expressing tumor antigens. T cells also produce tumor necrosis factor (TNF) and lymphotoxin, which promote inflammation. T cell mediated macrophage activation and inflammation may lead to tissue injury and this reaction is called delayed type hypersensitivity (DTH). Some chemicals introduced through skin bind to and modify the self-mhc proteins or molecules on the surface of APC, which are then recognized by CD8+ or CD4+ T lymphocytes. This type of DTH is called contact sensitivity. Role of CD4+ T cells: When protein antigens enter an individual, either they are captured by Langerhans cells in the skin (and similar cells in mucosa) and transported to draining lymph node or the antigen is drained to regional lymph node. The antigens are captured by dendritic cells in lymph nodes and presented on their surface with MHC proteins. During their migration to the regional draining lymph node, Langerhans cells express MHC class II molecules and mature into professional APCs, where they are called dendritic cells. Macrophages too engulf the foreign antigen, process it and present on their surfaces with MHC class II proteins. Presences of foreign antigen at the site of infection also induce innate immunity, which stimulates the APCs to express high levels of co-stimulators such as B7 proteins. Native T lymphocytes also migrate to the same peripheral lymphoid organ and encounter the processed antigen. After the naïve T cells encounter the antigen and receive the necessary co-stimulus, they secrete autocrine growth factor, IL-2. The cell then enters the cell cycle and the antigen-specific T cell clonally proliferates. Antigen specific CD8+ T cells also undergo clonal proliferation when they are suitably presented with antigen. Upon antigenic stimulation, T cells starts expressing CD40L in high numbers, which binds to CD40 expressed on the surface of APC. This stimulates the APC to start secreting IL-12. IFN-γ produced by NK cells during innate immune response also act on APC to induce IL-12 secretion. IL-12 acts on the activated T cells and induce the differentiation into Th1 subsets. Th1 effector cells produce IFN-γ, which acts on the APC resulting in increase in its microbicidal functions as well as further increase in IL-12 production. This results in further development of Th1 cells and thus provide an amplification of CMI. Some of the activated T cells develop into memory cells. Both the effector and memory cells leave the lymph and node and enter the circulation. To trigger the effector phase of CMI, effector or memory cells have to come in contact with APC presenting the antigens that initiated the response. If the response is against microbes that are ingested by macrophage in lymphoid organs, the effector T cells can locate the phagocyte in the same organ and activate them to kill the pathogen. If the infection is at some other location, the effector T cells leave circulation and enter the site of infection. Migration of leucocytes to sites of infection is stimulated by cytokines, which induce leucocyte chemotaxis and the expression of adhesion molecules on endothelial cells. Cytokines are produced by macrophages and endothelial cells that are stimulated by microbial products. Important cytokines participating in this process are the TNF and chemokines. TNF activates endothelial cells to express ligands for leucocyte adhesion molecules, resulting in attachment of leucocytes to the endothelium at the site of infection. Chemokines induce transendothelial migration of the attached leucocyte into the extravascular tissue. These cytokines are also produced by NK cells during innate immune reactions. An early inflammation characterized by leucocyte 3

4 influx may occur as part of innate immunity much before the T cell migration. After the T cells enter the site of infection and are activated by antigen, they stimulate much greater leucocyte migration. The effects of inflammation facilitates the migration and subsequent retention of leucocytes in the extravascular tissue. Previously activated effector and memory cells migrate preferentially to peripheral tissue at the site of infection because their migration is mediated by adhesion molecules, integrins and selectins. Activated T cells express ligands for selectins and express high levels of integrins. The endothelium at sites of infection express high levels of selectins and ligands for integrins. Once in the tissues, T cells encounter microbial antigens presented by APC. Once the T cell recognizes the antigen, the affinity of integrins to their ligands also increase. Two such integrins, VLA-4 and VLA-5 bind to fibronectin in extracellular matrix. Another adhesion molecule CD44, which is also expressed at high levels, binds to hyaluronate. As a result, antigen-specific T cells are preferentially retained at the site of infection. T cells not specific to the antigen returns via the lymphatic vessels to the circulation. Once the activated T cells encounter the specific antigen, they are further stimulated to perform their effector functions, which is to stimulate the microbicidal activities of macrophage. Monocytes that leave circulation and enter the site of infection are acted upon by the cytokines produced by effector T cells. This results in the conversion of inactive monocytes into activated macrophages that are able to engulf and kill microbes. The effector T cell that binds to the macrophage presenting the antigen activates it by production of IFN-γ and by binding of CD40L to macrophage s CD40. In response to CD40 signals and IFN-γ, production of several proteins in macrophage is increased. The effector functions of activated macrophages are: 1. Activated macrophages kill phagocytosed and extracellular microbes by producing microbicidal reactive oxygen intermediates, nitric oxide and lysosomal enzymes. 2. Activated macrophages stimulate acute inflammation through secretion of cytokines such as TNF, IL- 1 and chemokines. The result of this inflammation is to bring in neutrophils, which phagocytose and destroy pathogens. 3. Activated macrophages remove dead tissue and facilitate repair after the infection is controlled. They also secrete growth factors such as platelet-derived growth factor that stimulate fibroblast proliferation and transforming growth factor-β (TGF-β) that stimulate collagen synthesis. Tissue injury associated with CMI: Some tissue injury may normally accompany CMI reactions to microbes in the tissue because the microbicidal products released by the activated macrophages and neutrophils are capable of damaging normal tissue, and do not differentiate between microbes and host tissue. Usually, this tissue injury is limited in extent and duration, and it resolves as infection is cleared. If the activated macrophages fail to eradicate the infection, they continue to produce cytokine and growth factors, which progressively modify the local tissue environment. As a result, tissue injury is followed by replacement with connective tissue (fibrosis), and fibrosis is a hallmark of chronic DTH reactions. In chronic DTH reactions, activated macrophages also undergo changes in response to persistent cytokine signals. These macrophages develop increased cytoplasm and cytoplasmic organelles and histologically resemble skin epithelial cells because of which they are called epitheloid cells. Activated macrophages may fuse to form multinucleated giant cells. Clusters of activated macrophages, often surrounding particulate sources of antigen, produce nodules of inflammatory tissues called granulomas. Granulomatous inflammation is characteristic response to some persistent microbes, such as Mycobacterium tuberculosis and some fungi and represents a form of chronic DTH. Granulomatous inflammation is frequently associated with tissue fibrosis. Although fibrosis is normally a healing reaction to injury, it can also interfere with normal tissue function. 4

5 5

6 Role of CD8+ T cells: Cytotoxic T lymphocytes are effector T cells that recognize and kill target cells expressing foreign antigens in association with MHC proteins. The foreign antigen that is presented on the surface of the APC could be a viral protein, tumor protein or a bacterial protein that has escaped the lysosome and entered the cytosol. Most cytotoxic cells are CD8+ T cells that recognize antigen when presented with class I proteins. There are few CD4+ T cytotoxic cells that recognize antigen when presented with class II proteins. Differentiation of naïve CD8+ T cells to functional cytotoxic cells require the recognition of class I associated peptide antigen and co-stimulators (or cytokines). CD8+ T cells that leave the thymus after maturation and enter circulation or peripheral lymphoid organs are not fully differentiated to lyse target cells. These undifferentiated, functionally inactive CD8+ T cells are often called pre-ctls. First signals in the activation of pre-t cells into effector cytotoxic cells is the binding of TCR to peptide-class I proteins on APCs. Tumor cells or viral infected cells are often engulfed by macrophages, their antigens move from the phagosome into the cytosol and are presented in association with class I proteins. These professional APCs can provide co-stimulation for the T cells by the same they do for CD4+ T cells. The same antigen would also be processed and presented with class II proteins by APC to CD4+ T cells and activate them. Activated CD4+ T cells, if present in the vicinity of CD8+ T cells, provide cytokine signals that stimulate CD8+ T cells. Helper T cells produce IL-2, which stimulate the clonal proliferation of CD8+ T cells. Helper T cells bind to APC via CD40L and induce them to become more efficient at stimulating the differentiation of CD8+ T cells. Activation of CD8+ T cells by antigen along with second signal lead to their proliferation and differentiation into effector T cells capable of cytolytic functions. The most specific feature of cytotoxic cell differentiation is the development of membrane bound cytoplasmic granules that contain proteins, including perforins and granzymes. The differentiated cytotoxic cells also secrete IFN-γ, TNF and lymphotoxin, which activate phagocytes and induce inflammation. The effector cytotoxic cell binds to the target expressing the same 6

7 antigen with MHC class I molecule. TCR on the T cell binds to the peptide and CD8 of T cell binds to α3 chain of class I protein on APC. LFA-1 on T cell binds to ICAM-1 on APC. These signals are sufficient for activation of cytotoxic cell. Co-stimulators and cytokines that are required for the differentiation of pre-ctls into active CTLs are not necessary for triggering their effector functions. The principal mechanism of CTL-mediated cytolysis is the delivery of cytotoxic granule proteins to the target cell recognized by the CTL. The cytoplasmic granules of CTL fuses with the plasma membrane and releases the granules. The two most important granule proteins are perforins and granzymes. Perforin is a pore forming protein that is present as a monomer in the granules. When it is exocytosed fro the granules, the perforin monomer comes into contact with high concentration of calcium and undergoes polymerization. Polymerization of perforin occurs in the plasma membrane of target cell and thereby produce many large channels. The cell dies as a result of influx of water as well as apoptosis brought in by high levels of calcium. Granzymes are serine proteases which cleave proteins. They enter into the target cell through the pores created by perforins. Granzyme B proteolyticaly cleaves and activates cellular enzymes called caspases, which in turn cleave several substrates and induce apoptosis. CTLs use another mechanism of cytolysis that is mediated by interaction of membrane molecules on the CTLs and target cells. CTLs express a membrane protein called Fas ligand (FasL), which binds to its target protein Fas that is expressed in many cell types. This interaction also results in activation of caspases and apoptosis of the target cell. During the target cell cytolysis, the enzymatic cleavage occurs of host as well as microbial proteins and DNA. CTLs is then released from the target cell, which may be due to decrease in affinity of accessory molecules for their ligands. CTLS remain unaffected and usually disengage before the actual cytolysis occur. 7

8 Roles of Th2 cells in CMI The principal function of Th2 cells in CMI is to suppress the inflammatory reaction by cytokines that inhibit macrophage activation. Th2 cells secrete IL-4 and IL-13 that are antagonists of IFN-γ and thus block T cell mediated macrophage activation. Th2 cells also secrete IL-10, which directly inhibit macrophage activation. Th2 usually appear late in the immune response and the cytokine they produce perhaps play a role in limiting the damage brought about by CMI. Some Th2 cells also produce TGF-β, which suppress T cell proliferation and inhibit macrophages. Th2 cells also play a vital role in immunity to helminthic infections since they induce inflammatory reactions that are dominated by eosinophils and mast cells. Immune response to helminths largely consists of Th2 cells, which secrete IL-4 and IL-5. IL-4 stimulates the production of helminthic-specific IgE antibodies, which opsonize the helminths. IL-5 activates eosinophils, which bind to IgE coated on helminths. Degranulation of their contents leads to death of the helminth. Duration of CMI The functional response of T cells to antigen stimulation last only for few days or weeks, thereafter the response diminishes. Once the foreign antigen is eliminated after successful immune response, the T cell response by the effector cells also decline. The decline in T cell response is due to the death (apoptosis) of antigen-activated T cells. As the antigen is eliminated, the lymphocytes no longer get the survival stimuli that was provided by the antigen, the co-stimulators and the inflammatory cytokines. Some of the progeny of antigen-stimulated T cells survive and develop into antigen-specific memory T cells. Memory T cells survive for long periods even in the absence of continuous antigen exposure. The mechanism of memory cell survival is not known. These memory cells are responsible for enhanced and accelerated secondary immune response. Memory cells accumulate with age and it is believed that half of all T cells in adults are memory cells. Memory cells express high levels of integrins and CD44, which promote their migration to peripheral sites of infection and inflammation and their retention in those sites. This property enables the memory cells to rapidly locate and eliminate antigen at any site of infection or inflammation. Only upon re-exposure to the same antigen, memory cells proliferate and differentiate into effector cells. 8

T cell-mediated immunity

T cell-mediated immunity T cell-mediated immunity Overview For microbes within phagosomes in phagocytes.cd4+ T lymphocytes (TH1) Activate phagocyte by cytokines studies on Listeria monocytogenes For microbes infecting and replicating

More information

The Adaptive Immune Responses

The Adaptive Immune Responses The Adaptive Immune Responses The two arms of the immune responses are; 1) the cell mediated, and 2) the humoral responses. In this chapter we will discuss the two responses in detail and we will start

More information

Adaptive immune responses: T cell-mediated immunity

Adaptive immune responses: T cell-mediated immunity MICR2209 Adaptive immune responses: T cell-mediated immunity Dr Allison Imrie allison.imrie@uwa.edu.au 1 Synopsis: In this lecture we will discuss the T-cell mediated immune response, how it is activated,

More information

TCR, MHC and coreceptors

TCR, MHC and coreceptors Cooperation In Immune Responses Antigen processing how peptides get into MHC Antigen processing involves the intracellular proteolytic generation of MHC binding proteins Protein antigens may be processed

More information

C. Incorrect! MHC class I molecules are not involved in the process of bridging in ADCC.

C. Incorrect! MHC class I molecules are not involved in the process of bridging in ADCC. Immunology - Problem Drill 13: T- Cell Mediated Immunity Question No. 1 of 10 1. During Antibody-dependent cell mediated cytotoxicity (ADCC), the antibody acts like a bridge between the specific antigen

More information

Cellular Immune response. Jianzhong Chen, Ph.D Institute of immunology, ZJU

Cellular Immune response. Jianzhong Chen, Ph.D Institute of immunology, ZJU Cellular Immune response Jianzhong Chen, Ph.D Institute of immunology, ZJU Concept of adaptive immune response T cell-mediated adaptive immune response I. Concept of immune response A collective and coordinated

More information

Scott Abrams, Ph.D. Professor of Oncology, x4375 Kuby Immunology SEVENTH EDITION

Scott Abrams, Ph.D. Professor of Oncology, x4375 Kuby Immunology SEVENTH EDITION Scott Abrams, Ph.D. Professor of Oncology, x4375 scott.abrams@roswellpark.org Kuby Immunology SEVENTH EDITION CHAPTER 13 Effector Responses: Cell- and Antibody-Mediated Immunity Copyright 2013 by W. H.

More information

Effector mechanisms of cell-mediated immunity: Properties of effector, memory and regulatory T cells

Effector mechanisms of cell-mediated immunity: Properties of effector, memory and regulatory T cells ICI Basic Immunology course Effector mechanisms of cell-mediated immunity: Properties of effector, memory and regulatory T cells Abul K. Abbas, MD UCSF Stages in the development of T cell responses: induction

More information

ACTIVATION AND EFFECTOR FUNCTIONS OF CELL-MEDIATED IMMUNITY AND NK CELLS. Choompone Sakonwasun, MD (Hons), FRCPT

ACTIVATION AND EFFECTOR FUNCTIONS OF CELL-MEDIATED IMMUNITY AND NK CELLS. Choompone Sakonwasun, MD (Hons), FRCPT ACTIVATION AND EFFECTOR FUNCTIONS OF CELL-MEDIATED IMMUNITY AND NK CELLS Choompone Sakonwasun, MD (Hons), FRCPT Types of Adaptive Immunity Types of T Cell-mediated Immune Reactions CTLs = cytotoxic T lymphocytes

More information

Antigen Presentation and T Lymphocyte Activation. Abul K. Abbas UCSF. FOCiS

Antigen Presentation and T Lymphocyte Activation. Abul K. Abbas UCSF. FOCiS 1 Antigen Presentation and T Lymphocyte Activation Abul K. Abbas UCSF FOCiS 2 Lecture outline Dendritic cells and antigen presentation The role of the MHC T cell activation Costimulation, the B7:CD28 family

More information

Immunology. T-Lymphocytes. 16. Oktober 2014, Ruhr-Universität Bochum Karin Peters,

Immunology. T-Lymphocytes. 16. Oktober 2014, Ruhr-Universität Bochum Karin Peters, Immunology T-Lymphocytes 16. Oktober 2014, Ruhr-Universität Bochum Karin Peters, karin.peters@rub.de The role of T-effector cells in the immune response against microbes cellular immunity humoral immunity

More information

Defense mechanism against pathogens

Defense mechanism against pathogens Defense mechanism against pathogens Immune System What is immune system? Cells and organs within an animal s body that contribute to immune defenses against pathogens ( ) Bacteria -Major entry points ;open

More information

chapter 17: specific/adaptable defenses of the host: the immune response

chapter 17: specific/adaptable defenses of the host: the immune response chapter 17: specific/adaptable defenses of the host: the immune response defense against infection & illness body defenses innate/ non-specific adaptable/ specific epithelium, fever, inflammation, complement,

More information

The T cell receptor for MHC-associated peptide antigens

The T cell receptor for MHC-associated peptide antigens 1 The T cell receptor for MHC-associated peptide antigens T lymphocytes have a dual specificity: they recognize polymporphic residues of self MHC molecules, and they also recognize residues of peptide

More information

Immune response. This overview figure summarizes simply how our body responds to foreign molecules that enter to it.

Immune response. This overview figure summarizes simply how our body responds to foreign molecules that enter to it. Immune response This overview figure summarizes simply how our body responds to foreign molecules that enter to it. It s highly recommended to watch Dr Najeeb s lecture that s titled T Helper cells and

More information

Test Bank for Basic Immunology Functions and Disorders of the Immune System 4th Edition by Abbas

Test Bank for Basic Immunology Functions and Disorders of the Immune System 4th Edition by Abbas Test Bank for Basic Immunology Functions and Disorders of the Immune System 4th Edition by Abbas Chapter 04: Antigen Recognition in the Adaptive Immune System Test Bank MULTIPLE CHOICE 1. Most T lymphocytes

More information

Cell Mediated Immunity CELL MEDIATED IMMUNITY. Basic Elements of Cell Mediated Immunity (CMI) Antibody-dependent cell-mediated cytotoxicity (ADCC)

Cell Mediated Immunity CELL MEDIATED IMMUNITY. Basic Elements of Cell Mediated Immunity (CMI) Antibody-dependent cell-mediated cytotoxicity (ADCC) Chapter 16 CELL MEDIATED IMMUNITY Cell Mediated Immunity Also known as Cellular Immunity or CMI The effector phase T cells Specificity for immune recognition reactions TH provide cytokines CTLs do the

More information

T Cell Effector Mechanisms I: B cell Help & DTH

T Cell Effector Mechanisms I: B cell Help & DTH T Cell Effector Mechanisms I: B cell Help & DTH Ned Braunstein, MD The Major T Cell Subsets p56 lck + T cells γ δ ε ζ ζ p56 lck CD8+ T cells γ δ ε ζ ζ Cα Cβ Vα Vβ CD3 CD8 Cα Cβ Vα Vβ CD3 MHC II peptide

More information

Defensive mechanisms include :

Defensive mechanisms include : Acquired Immunity Defensive mechanisms include : 1) Innate immunity (Natural or Non specific) 2) Acquired immunity (Adaptive or Specific) Cell-mediated immunity Humoral immunity Two mechanisms 1) Humoral

More information

محاضرة مناعت مدرس المادة :ا.م. هدى عبدالهادي علي النصراوي Immunity to Infectious Diseases

محاضرة مناعت مدرس المادة :ا.م. هدى عبدالهادي علي النصراوي Immunity to Infectious Diseases محاضرة مناعت مدرس المادة :ا.م. هدى عبدالهادي علي النصراوي Immunity to Infectious Diseases Immunity to infection depends on a combination of innate mechanisms (phagocytosis, complement, etc.) and antigen

More information

Medical Virology Immunology. Dr. Sameer Naji, MB, BCh, PhD (UK) Head of Basic Medical Sciences Dept. Faculty of Medicine The Hashemite University

Medical Virology Immunology. Dr. Sameer Naji, MB, BCh, PhD (UK) Head of Basic Medical Sciences Dept. Faculty of Medicine The Hashemite University Medical Virology Immunology Dr. Sameer Naji, MB, BCh, PhD (UK) Head of Basic Medical Sciences Dept. Faculty of Medicine The Hashemite University Human blood cells Phases of immune responses Microbe Naïve

More information

Chapter 10 (pages ): Differentiation and Functions of CD4+ Effector T Cells Prepared by Kristen Dazy, MD, Scripps Clinic Medical Group

Chapter 10 (pages ): Differentiation and Functions of CD4+ Effector T Cells Prepared by Kristen Dazy, MD, Scripps Clinic Medical Group FIT Board Review Corner September 2015 Welcome to the FIT Board Review Corner, prepared by Andrew Nickels, MD, and Sarah Spriet, DO, senior and junior representatives of ACAAI's Fellows-In-Training (FITs)

More information

Topics. Humoral Immune Response Part II Accessory cells Fc Receptors Opsonization and killing mechanisms of phagocytes NK, mast, eosynophils

Topics. Humoral Immune Response Part II Accessory cells Fc Receptors Opsonization and killing mechanisms of phagocytes NK, mast, eosynophils Topics Humoral Immune Response Part II Accessory cells Fc Receptors Opsonization and killing mechanisms of phagocytes NK, mast, eosynophils Immune regulation Idiotypic network 2/15/2005 MICR 415 / 515

More information

1. Overview of Adaptive Immunity

1. Overview of Adaptive Immunity Chapter 17A: Adaptive Immunity Part I 1. Overview of Adaptive Immunity 2. T and B Cell Production 3. Antigens & Antigen Presentation 4. Helper T cells 1. Overview of Adaptive Immunity The Nature of Adaptive

More information

Properties & Overview of IRs Dr. Nasser M. Kaplan JUST, Jordan. 10-Jul-16 NM Kaplan 1

Properties & Overview of IRs Dr. Nasser M. Kaplan JUST, Jordan. 10-Jul-16 NM Kaplan 1 Properties & Overview of IRs Dr. Nasser M. Kaplan JUST, Jordan 10-Jul-16 NM Kaplan 1 Major components of IS & their properties Definitions IS = cells & molecules responsible for: 1- Physiologic; protective

More information

Immunology - Lecture 2 Adaptive Immune System 1

Immunology - Lecture 2 Adaptive Immune System 1 Immunology - Lecture 2 Adaptive Immune System 1 Book chapters: Molecules of the Adaptive Immunity 6 Adaptive Cells and Organs 7 Generation of Immune Diversity Lymphocyte Antigen Receptors - 8 CD markers

More information

Effector T Cells and

Effector T Cells and 1 Effector T Cells and Cytokines Andrew Lichtman, MD PhD Brigham and Women's Hospital Harvard Medical School 2 Lecture outline Cytokines Subsets of CD4+ T cells: definitions, functions, development New

More information

Immune response to infection

Immune response to infection Immune response to infection Dr. Sandra Nitsche (Sandra.Nitsche@rub.de ) 20.06.2018 1 Course of acute infection Typical acute infection that is cleared by an adaptive immune reaction 1. invasion of pathogen

More information

Effector Mechanisms of Cell-Mediated Immunity

Effector Mechanisms of Cell-Mediated Immunity Effector Mechanisms of Cell-Mediated Immunity Dr. Julia Rempel Section of Hepatology 789-3825 jdrempel@cc.umanitoba.ca 804D JBRC Topics: I. Types of Cell-Mediated Immunity II. Migration of Effector T Lymphocytes

More information

CELL BIOLOGY - CLUTCH CH THE IMMUNE SYSTEM.

CELL BIOLOGY - CLUTCH CH THE IMMUNE SYSTEM. !! www.clutchprep.com CONCEPT: OVERVIEW OF HOST DEFENSES The human body contains three lines of against infectious agents (pathogens) 1. Mechanical and chemical boundaries (part of the innate immune system)

More information

Chapter 17B: Adaptive Immunity Part II

Chapter 17B: Adaptive Immunity Part II Chapter 17B: Adaptive Immunity Part II 1. Cell-Mediated Immune Response 2. Humoral Immune Response 3. Antibodies 1. The Cell-Mediated Immune Response Basic Steps of Cell-Mediated IR 1 2a CD4 + MHC cl.

More information

The Immune System. These are classified as the Innate and Adaptive Immune Responses. Innate Immunity

The Immune System. These are classified as the Innate and Adaptive Immune Responses. Innate Immunity The Immune System Biological mechanisms that defend an organism must be 1. triggered by a stimulus upon injury or pathogen attack 2. able to counteract the injury or invasion 3. able to recognise foreign

More information

The Immune System: Innate and Adaptive Body Defenses Outline PART 1: INNATE DEFENSES 21.1 Surface barriers act as the first line of defense to keep

The Immune System: Innate and Adaptive Body Defenses Outline PART 1: INNATE DEFENSES 21.1 Surface barriers act as the first line of defense to keep The Immune System: Innate and Adaptive Body Defenses Outline PART 1: INNATE DEFENSES 21.1 Surface barriers act as the first line of defense to keep invaders out of the body (pp. 772 773; Fig. 21.1; Table

More information

General Overview of Immunology. Kimberly S. Schluns, Ph.D. Associate Professor Department of Immunology UT MD Anderson Cancer Center

General Overview of Immunology. Kimberly S. Schluns, Ph.D. Associate Professor Department of Immunology UT MD Anderson Cancer Center General Overview of Immunology Kimberly S. Schluns, Ph.D. Associate Professor Department of Immunology UT MD Anderson Cancer Center Objectives Describe differences between innate and adaptive immune responses

More information

WHY IS THIS IMPORTANT?

WHY IS THIS IMPORTANT? CHAPTER 16 THE ADAPTIVE IMMUNE RESPONSE WHY IS THIS IMPORTANT? The adaptive immune system protects us from many infections The adaptive immune system has memory so we are not infected by the same pathogen

More information

Micro 204. Cytotoxic T Lymphocytes (CTL) Lewis Lanier

Micro 204. Cytotoxic T Lymphocytes (CTL) Lewis Lanier Micro 204 Cytotoxic T Lymphocytes (CTL) Lewis Lanier Lewis.Lanier@ucsf.edu Lymphocyte-mediated Cytotoxicity CD8 + αβ-tcr + T cells CD4 + αβ-tcr + T cells γδ-tcr + T cells Natural Killer cells CD8 + αβ-tcr

More information

The Adaptive Immune Response. B-cells

The Adaptive Immune Response. B-cells The Adaptive Immune Response B-cells The innate immune system provides immediate protection. The adaptive response takes time to develop and is antigen specific. Activation of B and T lymphocytes Naive

More information

Immunology for the Rheumatologist

Immunology for the Rheumatologist Immunology for the Rheumatologist Rheumatologists frequently deal with the immune system gone awry, rarely studying normal immunology. This program is an overview and discussion of the function of the

More information

Immune System AP SBI4UP

Immune System AP SBI4UP Immune System AP SBI4UP TYPES OF IMMUNITY INNATE IMMUNITY ACQUIRED IMMUNITY EXTERNAL DEFENCES INTERNAL DEFENCES HUMORAL RESPONSE Skin Phagocytic Cells CELL- MEDIATED RESPONSE Mucus layer Antimicrobial

More information

General Biology. A summary of innate and acquired immunity. 11. The Immune System. Repetition. The Lymphatic System. Course No: BNG2003 Credits: 3.

General Biology. A summary of innate and acquired immunity. 11. The Immune System. Repetition. The Lymphatic System. Course No: BNG2003 Credits: 3. A summary of innate and acquired immunity General iology INNATE IMMUNITY Rapid responses to a broad range of microbes Course No: NG00 Credits:.00 External defenses Invading microbes (pathogens). The Immune

More information

Clinical Basis of the Immune Response and the Complement Cascade

Clinical Basis of the Immune Response and the Complement Cascade Clinical Basis of the Immune Response and the Complement Cascade Bryan L. Martin, DO, MMAS, FACAAI, FAAAAI, FACOI, FACP Emeritus Professor of Medicine and Pediatrics President, American College of Allergy,

More information

M.Sc. III Semester Biotechnology End Semester Examination, 2013 Model Answer LBTM: 302 Advanced Immunology

M.Sc. III Semester Biotechnology End Semester Examination, 2013 Model Answer LBTM: 302 Advanced Immunology Code : AS-2246 M.Sc. III Semester Biotechnology End Semester Examination, 2013 Model Answer LBTM: 302 Advanced Immunology A. Select one correct option for each of the following questions:- 2X10=10 1. (b)

More information

Introduction to Immunology Lectures 1-3 by Bellur S. Prabhakar. March 13-14, 2007

Introduction to Immunology Lectures 1-3 by Bellur S. Prabhakar. March 13-14, 2007 Introduction to Immunology Lectures 1-3 by Bellur S. Prabhakar. March 13-14, 2007 TheComponents Of The Immune System and Innate Immunity: Ref: Immunobiology-5 th edition. Janeway et al. Chapters-1 & 2.

More information

number Done by Corrected by Doctor Mousa Al-Abbadi

number Done by Corrected by Doctor Mousa Al-Abbadi number 11 Done by Husam Abu-Awad Corrected by Muhammad Tarabieh Doctor Mousa Al-Abbadi The possible outcomes of an acute inflammation are the following: 1- A complete resolution in which the tissue returns

More information

Hematopoiesis. Hematopoiesis. Hematopoiesis

Hematopoiesis. Hematopoiesis. Hematopoiesis Chapter. Cells and Organs of the Immune System Hematopoiesis Hematopoiesis- formation and development of WBC and RBC bone marrow. Hematopoietic stem cell- give rise to any blood cells (constant number,

More information

Prof. Ibtesam Kamel Afifi Professor of Medical Microbiology & Immunology

Prof. Ibtesam Kamel Afifi Professor of Medical Microbiology & Immunology By Prof. Ibtesam Kamel Afifi Professor of Medical Microbiology & Immunology Lecture objectives: At the end of the lecture you should be able to: Enumerate features that characterize acquired immune response

More information

Time course of immune response

Time course of immune response Time course of immune response Route of entry Route of entry (cont.) Steps in infection Barriers to infection Mf receptors Facilitate engulfment Glucan, mannose Scavenger CD11b/CD18 Allows immediate response

More information

Immunology Basics Relevant to Cancer Immunotherapy: T Cell Activation, Costimulation, and Effector T Cells

Immunology Basics Relevant to Cancer Immunotherapy: T Cell Activation, Costimulation, and Effector T Cells Immunology Basics Relevant to Cancer Immunotherapy: T Cell Activation, Costimulation, and Effector T Cells Andrew H. Lichtman, M.D. Ph.D. Department of Pathology Brigham and Women s Hospital and Harvard

More information

5/1/13. The proportion of thymus that produces T cells decreases with age. The cellular organization of the thymus

5/1/13. The proportion of thymus that produces T cells decreases with age. The cellular organization of the thymus T cell precursors migrate from the bone marrow via the blood to the thymus to mature 1 2 The cellular organization of the thymus The proportion of thymus that produces T cells decreases with age 3 4 1

More information

Nonspecific External Barriers skin, mucous membranes

Nonspecific External Barriers skin, mucous membranes Immune system Chapter 36 BI 103 Plant-Animal A&P Levels of Defense Against Disease Nonspecific External Barriers skin, mucous membranes Physical barriers? Brainstorm with a partner If these barriers are

More information

The development of T cells in the thymus

The development of T cells in the thymus T cells rearrange their receptors in the thymus whereas B cells do so in the bone marrow. The development of T cells in the thymus The lobular/cellular organization of the thymus Immature cells are called

More information

Anti-infectious Immunity

Anti-infectious Immunity Anti-infectious Immunity innate immunity barrier structures Secretory molecules Phagocytes NK cells Anatomical barriers 1. Skin and mucosa barrier 2.hemo-Spinal Fluid barrier 3. placental barrier Phagocytic

More information

T-cell activation T cells migrate to secondary lymphoid tissues where they interact with antigen, antigen-presenting cells, and other lymphocytes:

T-cell activation T cells migrate to secondary lymphoid tissues where they interact with antigen, antigen-presenting cells, and other lymphocytes: Interactions between innate immunity & adaptive immunity What happens to T cells after they leave the thymus? Naïve T cells exit the thymus and enter the bloodstream. If they remain in the bloodstream,

More information

T-cell activation T cells migrate to secondary lymphoid tissues where they interact with antigen, antigen-presenting cells, and other lymphocytes:

T-cell activation T cells migrate to secondary lymphoid tissues where they interact with antigen, antigen-presenting cells, and other lymphocytes: Interactions between innate immunity & adaptive immunity What happens to T cells after they leave the thymus? Naïve T cells exit the thymus and enter the bloodstream. If they remain in the bloodstream,

More information

The Major Histocompatibility Complex (MHC)

The Major Histocompatibility Complex (MHC) The Major Histocompatibility Complex (MHC) An introduction to adaptive immune system before we discuss MHC B cells The main cells of adaptive immune system are: -B cells -T cells B cells: Recognize antigens

More information

ANATOMY OF THE IMMUNE SYSTEM

ANATOMY OF THE IMMUNE SYSTEM Immunity Learning objectives Explain what triggers an immune response and where in the body the immune response occurs. Understand how the immune system handles exogenous and endogenous antigen differently.

More information

The Innate Immune Response

The Innate Immune Response The Innate Immune Response FUNCTIONS OF THE IMMUNE SYSTEM: Recognize, destroy and clear a diversity of pathogens. Initiate tissue and wound healing processes. Recognize and clear damaged self components.

More information

Immune system. Aims. Immune system. Lymphatic organs. Inflammation. Natural immune system. Adaptive immune system

Immune system. Aims. Immune system. Lymphatic organs. Inflammation. Natural immune system. Adaptive immune system Aims Immune system Lymphatic organs Inflammation Natural immune system Adaptive immune system Major histocompatibility complex (MHC) Disorders of the immune system 1 2 Immune system Lymphoid organs Immune

More information

LESSON 2: THE ADAPTIVE IMMUNITY

LESSON 2: THE ADAPTIVE IMMUNITY Introduction to immunology. LESSON 2: THE ADAPTIVE IMMUNITY Today we will get to know: The adaptive immunity T- and B-cells Antigens and their recognition How T-cells work 1 The adaptive immunity Unlike

More information

Principles of Adaptive Immunity

Principles of Adaptive Immunity Principles of Adaptive Immunity Chapter 3 Parham Hans de Haard 17 th of May 2010 Agenda Recognition molecules of adaptive immune system Features adaptive immune system Immunoglobulins and T-cell receptors

More information

Overview of the Lymphoid System

Overview of the Lymphoid System Overview of the Lymphoid System The Lymphoid System Protects us against disease Lymphoid system cells respond to Environmental pathogens Toxins Abnormal body cells, such as cancers Overview of the Lymphoid

More information

The Adaptive Immune Response: T lymphocytes and Their Functional Types *

The Adaptive Immune Response: T lymphocytes and Their Functional Types * OpenStax-CNX module: m46560 1 The Adaptive Immune Response: T lymphocytes and Their Functional Types * OpenStax This work is produced by OpenStax-CNX and licensed under the Creative Commons Attribution

More information

Chapter 1. Chapter 1 Concepts. MCMP422 Immunology and Biologics Immunology is important personally and professionally!

Chapter 1. Chapter 1 Concepts. MCMP422 Immunology and Biologics Immunology is important personally and professionally! MCMP422 Immunology and Biologics Immunology is important personally and professionally! Learn the language - use the glossary and index RNR - Reading, Note taking, Reviewing All materials in Chapters 1-3

More information

Question 1. Kupffer cells, microglial cells and osteoclasts are all examples of what type of immune system cell?

Question 1. Kupffer cells, microglial cells and osteoclasts are all examples of what type of immune system cell? Abbas Chapter 2: Sarah Spriet February 8, 2015 Question 1. Kupffer cells, microglial cells and osteoclasts are all examples of what type of immune system cell? a. Dendritic cells b. Macrophages c. Monocytes

More information

remember that T-cell signal determine what antibody to be produce class switching somatical hypermutation all takes place after interaction with

remember that T-cell signal determine what antibody to be produce class switching somatical hypermutation all takes place after interaction with بسم هللا الرحمن الرحيم The last lecture we discussed the antigen processing and presentation and antigen recognition then the activation by T lymphocyte and today we will continue with B cell recognition

More information

Physiology Unit 3. ADAPTIVE IMMUNITY The Specific Immune Response

Physiology Unit 3. ADAPTIVE IMMUNITY The Specific Immune Response Physiology Unit 3 ADAPTIVE IMMUNITY The Specific Immune Response In Physiology Today The Adaptive Arm of the Immune System Specific Immune Response Internal defense against a specific pathogen Acquired

More information

Overview of the immune system

Overview of the immune system Overview of the immune system Immune system Innate (nonspecific) 1 st line of defense Adaptive (specific) 2 nd line of defense Cellular components Humoral components Cellular components Humoral components

More information

1. The scavenger receptor, CD36, functions as a coreceptor for which TLR? a. TLR ½ b. TLR 3 c. TLR 4 d. TLR 2/6

1. The scavenger receptor, CD36, functions as a coreceptor for which TLR? a. TLR ½ b. TLR 3 c. TLR 4 d. TLR 2/6 Allergy and Immunology Review Corner: Cellular and Molecular Immunology, 8th Edition By Abul K. Abbas, MBBS, Andrew H. H. Lichtman, MD, PhD and Shiv Pillai, MBBS, PhD. Chapter 4 (pages 62-74): Innate Immunity

More information

All animals have innate immunity, a defense active immediately upon infection Vertebrates also have adaptive immunity

All animals have innate immunity, a defense active immediately upon infection Vertebrates also have adaptive immunity 1 2 3 4 5 6 7 8 9 The Immune System All animals have innate immunity, a defense active immediately upon infection Vertebrates also have adaptive immunity Figure 43.2 In innate immunity, recognition and

More information

immunity defenses invertebrates vertebrates chapter 48 Animal defenses --

immunity defenses invertebrates vertebrates chapter 48 Animal defenses -- defenses Animal defenses -- immunity chapter 48 invertebrates coelomocytes, amoebocytes, hemocytes sponges, cnidarians, etc. annelids basophilic amoebocytes, acidophilic granulocytes arthropod immune systems

More information

Chapter 22: The Lymphatic System and Immunity

Chapter 22: The Lymphatic System and Immunity Bio40C schedule Lecture Immune system Lab Quiz 2 this week; bring a scantron! Study guide on my website (see lab assignments) Extra credit Critical thinking questions at end of chapters 5 pts/chapter Due

More information

T cell and Cell-mediated immunity

T cell and Cell-mediated immunity T cell and Cell-mediated immunity ( 第十章 第十二章第十二章 ) Lu Linrong ( 鲁林荣 ) PhD Laboratory of Immune Regulation Institute of Immunology Zhejiang University, School of Medicine Medical Research Building B815-819

More information

The recruitment of leukocytes and plasma proteins from the blood to sites of infection and tissue injury is called inflammation

The recruitment of leukocytes and plasma proteins from the blood to sites of infection and tissue injury is called inflammation The migration of a particular type of leukocyte into a restricted type of tissue, or a tissue with an ongoing infection or injury, is often called leukocyte homing, and the general process of leukocyte

More information

Adaptive Immunity. Jeffrey K. Actor, Ph.D. MSB 2.214,

Adaptive Immunity. Jeffrey K. Actor, Ph.D. MSB 2.214, Adaptive Immunity Jeffrey K. Actor, Ph.D. MSB 2.214, 500-5344 Lecture Objectives: Understand role of various molecules including cytokines, chemokines, costimulatory and adhesion molecules in the development

More information

Follicular Lymphoma. ced3 APOPTOSIS. *In the nematode Caenorhabditis elegans 131 of the organism's 1031 cells die during development.

Follicular Lymphoma. ced3 APOPTOSIS. *In the nematode Caenorhabditis elegans 131 of the organism's 1031 cells die during development. Harvard-MIT Division of Health Sciences and Technology HST.176: Cellular and Molecular Immunology Course Director: Dr. Shiv Pillai Follicular Lymphoma 1. Characterized by t(14:18) translocation 2. Ig heavy

More information

Chapter 13 Lymphatic and Immune Systems

Chapter 13 Lymphatic and Immune Systems The Chapter 13 Lymphatic and Immune Systems 1 The Lymphatic Vessels Lymphoid Organs Three functions contribute to homeostasis 1. Return excess tissue fluid to the bloodstream 2. Help defend the body against

More information

Structure and Function of Antigen Recognition Molecules

Structure and Function of Antigen Recognition Molecules MICR2209 Structure and Function of Antigen Recognition Molecules Dr Allison Imrie allison.imrie@uwa.edu.au 1 Synopsis: In this lecture we will examine the major receptors used by cells of the innate and

More information

Adaptive Immunity: Humoral Immune Responses

Adaptive Immunity: Humoral Immune Responses MICR2209 Adaptive Immunity: Humoral Immune Responses Dr Allison Imrie 1 Synopsis: In this lecture we will review the different mechanisms which constitute the humoral immune response, and examine the antibody

More information

Adaptive Immunity: Specific Defenses of the Host

Adaptive Immunity: Specific Defenses of the Host 17 Adaptive Immunity: Specific Defenses of the Host SLOs Differentiate between innate and adaptive immunity, and humoral and cellular immunity. Define antigen, epitope, and hapten. Explain the function

More information

VMC-221: Veterinary Immunology and Serology (1+1) Question Bank

VMC-221: Veterinary Immunology and Serology (1+1) Question Bank VMC-221: Veterinary Immunology and Serology (1+1) Objective type Questions Question Bank Q. No. 1 - Fill up the blanks with correct words 1. The British physician, who developed the first vaccine against

More information

Introduction to Immunopathology

Introduction to Immunopathology MICR2209 Introduction to Immunopathology Dr Allison Imrie 1 Allergy and Hypersensitivity Adaptive immune responses can sometimes be elicited by antigens not associated with infectious agents, and this

More information

There are 2 major lines of defense: Non-specific (Innate Immunity) and. Specific. (Adaptive Immunity) Photo of macrophage cell

There are 2 major lines of defense: Non-specific (Innate Immunity) and. Specific. (Adaptive Immunity) Photo of macrophage cell There are 2 major lines of defense: Non-specific (Innate Immunity) and Specific (Adaptive Immunity) Photo of macrophage cell Development of the Immune System ery pl neu mφ nk CD8 + CTL CD4 + thy TH1 mye

More information

Adaptive Immunity. PowerPoint Lecture Presentations prepared by Mindy Miller-Kittrell, North Carolina State University C H A P T E R

Adaptive Immunity. PowerPoint Lecture Presentations prepared by Mindy Miller-Kittrell, North Carolina State University C H A P T E R CSLO7. Describe functions of host defenses and the immune system in combating infectious diseases and explain how immunizations protect against specific diseases. PowerPoint Lecture Presentations prepared

More information

Lymphoid System: cells of the immune system. Answer Sheet

Lymphoid System: cells of the immune system. Answer Sheet Lymphoid System: cells of the immune system Answer Sheet Q1 Which areas of the lymph node have most CD3 staining? A1 Most CD3 staining is present in the paracortex (T cell areas). This is towards the outside

More information

T cell and Cell-mediated immunity

T cell and Cell-mediated immunity T cell and Cell-mediated immunity Lu Linrong ( 鲁林荣 ) PhD Laboratory of Immune Regulation Institute of Immunology Zhejiang University, it School of Medicine i Medical Research Building B815-819 Email: Lu.Linrong@gmail.com

More information

Innate vs Adaptive Response

Innate vs Adaptive Response General Immunology Innate vs Adaptive Response Innate- non-specific (4 types of barriers) anatomic- ato mechanical ca (skin), ph, mucous, normal flora Physiologic- temperature, ph, chemicals (lysozyme,

More information

Chapter 23 Immunity Exam Study Questions

Chapter 23 Immunity Exam Study Questions Chapter 23 Immunity Exam Study Questions 1. Define 1) Immunity 2) Neutrophils 3) Macrophage 4) Epitopes 5) Interferon 6) Complement system 7) Histamine 8) Mast cells 9) Antigen 10) Antigens receptors 11)

More information

Third line of Defense

Third line of Defense Chapter 15 Specific Immunity and Immunization Topics -3 rd of Defense - B cells - T cells - Specific Immunities Third line of Defense Specific immunity is a complex interaction of immune cells (leukocytes)

More information

T Lymphocyte Activation and Costimulation. FOCiS. Lecture outline

T Lymphocyte Activation and Costimulation. FOCiS. Lecture outline 1 T Lymphocyte Activation and Costimulation Abul K. Abbas, MD UCSF FOCiS 2 Lecture outline T cell activation Costimulation, the B7:CD28 family Inhibitory receptors of T cells Targeting costimulators for

More information

Adaptive Immunity. PowerPoint Lecture Presentations prepared by Mindy Miller-Kittrell, North Carolina State University C H A P T E R

Adaptive Immunity. PowerPoint Lecture Presentations prepared by Mindy Miller-Kittrell, North Carolina State University C H A P T E R PowerPoint Lecture Presentations prepared by Mindy Miller-Kittrell, North Carolina State University C H A P T E R 16 Adaptive Immunity The Body s Third Line of Defense Adaptive Immunity Adaptive immunity

More information

Chapter 3, Part A (Pages 37-45): Leukocyte Migration into Tissues

Chapter 3, Part A (Pages 37-45): Leukocyte Migration into Tissues Allergy and Immunology Review Corner: Chapter 3, Part A (pages 37-45) of Cellular and Molecular Immunology (Seventh Edition), by Abul K. Abbas, Andrew H. Lichtman and Shiv Pillai. Chapter 3, Part A (Pages

More information

Immunity. Acquired immunity differs from innate immunity in specificity & memory from 1 st exposure

Immunity. Acquired immunity differs from innate immunity in specificity & memory from 1 st exposure Immunity (1) Non specific (innate) immunity (2) Specific (acquired) immunity Characters: (1) Non specific: does not need special recognition of the foreign cell. (2) Innate: does not need previous exposure.

More information

Adaptive (acquired) immunity. Professor Peter Delves University College London

Adaptive (acquired) immunity. Professor Peter Delves University College London Adaptive (acquired) immunity Professor Peter Delves University College London p.delves@ucl.ac.uk Haematopoiesis Haematopoiesis Lymphocytes = adaptive response Recognition of pathogens by adaptive cells,

More information

Basis of Immunology and

Basis of Immunology and Basis of Immunology and Immunophysiopathology of Infectious Diseases Jointly organized by Institut Pasteur in Ho Chi Minh City and Institut Pasteur with kind support from ANRS & Université Pierre et Marie

More information

Cell-mediated Immunity

Cell-mediated Immunity Cellular & Molecular Immunology Cell-mediated Immunity Nicholas M. Ponzio, Ph.D. Department of Pathology & Laboratory Medicine April 6, 2009 Today s Presentation: Overview Cellular Interactions In Humoral

More information

Objectives. Abbas Chapter 11: Immunological Tolerance. Question 1. Question 2. Question 3. Definitions

Objectives. Abbas Chapter 11: Immunological Tolerance. Question 1. Question 2. Question 3. Definitions Objectives Abbas Chapter 11: Immunological Tolerance Christina Ciaccio, MD Children s Mercy Hospitals and Clinics February 1, 2010 To introduce the concept of immunologic tolerance To understand what factors

More information

Innate Immunity. Natural or native immunity

Innate Immunity. Natural or native immunity Innate Immunity 1 Innate Immunity Natural or native immunity 2 When microbes enter in the body 3 Secondly, it also stimulates the adaptive immune system 4 Immunologic memory 5 Components of Innate Immunity

More information

I. Lines of Defense Pathogen: Table 1: Types of Immune Mechanisms. Table 2: Innate Immunity: First Lines of Defense

I. Lines of Defense Pathogen: Table 1: Types of Immune Mechanisms. Table 2: Innate Immunity: First Lines of Defense I. Lines of Defense Pathogen: Table 1: Types of Immune Mechanisms Table 2: Innate Immunity: First Lines of Defense Innate Immunity involves nonspecific physical & chemical barriers that are adapted for

More information

MACROPHAGE "MONOCYTES" SURFACE RECEPTORS

MACROPHAGE MONOCYTES SURFACE RECEPTORS LECTURE: 13 Title: MACROPHAGE "MONOCYTES" SURFACE RECEPTORS LEARNING OBJECTIVES: The student should be able to: Describe the blood monocytes (size, and shape of nucleus). Enumerate some of the monocytes

More information

Slide 1. Slide 2. Slide 3 IMMUNOLOGY AND THE PATHOPHYSIOLOGY OF INFECTION

Slide 1. Slide 2. Slide 3 IMMUNOLOGY AND THE PATHOPHYSIOLOGY OF INFECTION Slide 1 IMMUNOLOGY AND THE PATHOPHYSIOLOGY OF INFECTION Pharmacotherapy of Infectious Diseases 5214 Slide 2 IMMUNE SYSTEM A network of cells, tissues and organs that work together to protect the body against

More information