2014 Pearson Education, Inc. CHAPTER 15 Innate Immunity

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1 CHAPTER 15 Innate Immunity

2 An Overview of the Body's Defenses Resistance to most plant and animal pathogens Species resistance Due to physiological processes of humans that are incompatible with those of the pathogen Correct chemical receptors not present on human cells Conditions may be incompatible with those needed for pathogen's survival Humans don't have innate resistance to a number of pathogens

3 Host Defenses: Overview

4 The Body's First Line of Defense Structures, chemicals, and processes that work to prevent pathogens entering the body Skin and mucous membranes of the respiratory, digestive, urinary, and reproductive systems

5 The Body's First Line of Defense The Role of Skin in Innate Immunity Skin composed of two major layers Epidermis Multiple layers of tightly packed cells Few pathogens can penetrate these layers Shedding of dead skin cells removes microorganisms Epidermal dendritic cells phagocytize pathogens Dermis Collagen fibers help skin resist abrasions that could introduce microorganisms

6 The Body's First Line of Defense The Role of Skin in Innate Immunity Skin has chemicals that defend against pathogens Perspiration secreted by sweat glands Salt inhibits growth of pathogens Antimicrobial peptides act against microorganisms Lysozyme destroys cell wall of bacteria Sebum secreted by sebaceous (oil) glands Helps keep skin pliable and less likely to break or tear Lowers skin ph to a level inhibitory to many bacteria

7 The Body's First Line of Defense The Role of Mucous Membranes in Innate Immunity Mucous membranes line all body cavities open to environment Two distinct layers Epithelium Thin, outer covering of the mucous membranes Epithelial cells are living Tightly packed to prevent entry of many pathogens Continual shedding of cells carries away microorganisms Dendritic cells below epithelium phagocytize pathogens Goblet and ciliated columnar cells help remove invaders Deeper connective layer that supports the epithelium Produce chemicals that defend against pathogens

8 Figure 15.2 The structure of the respiratory system, which is lined with a mucous membrane. Nasal cavity Pharynx Tongue Epiglottis Larynx (voice box) Esophagus Trachea Bronchus Bronchioles

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10 The Body's First Line of Defense The Role of the Lacrimal Apparatus in Innate Immunity Lacrimal apparatus Produces and drains tears Blinking spreads tears and washes surface of the eye Lysozyme in tears destroys bacteria

11 Figure 15.3 The lacrimal apparatus. Nasolacrimal duct Lacrimal apparatus Nasolacrimal duct Lacrimal canal Lacrimal glands Lacrimal gland duct Paranasal sinus Pharynx Trachea Esophagus Anterior view Lateral view

12 The Body's First Line of Defense The Role of Normal Microbiota in Innate Immunity Microbial antagonism Normal microbiota compete with potential pathogens Activities of normal microbiota make it hard for pathogens to compete Consumption of nutrients Create an environment unfavorable to other microorganisms Help stimulate the body's second line of defense Promote overall health by providing vitamins to host

13 The Body's First Line of Defense Other First-Line Defenses Antimicrobial peptides Present in skin, mucous membranes, neutrophils Act against a variety of microbes Work in several ways Other processes and chemicals Many organs secrete chemicals with antimicrobial properties

14 The Body's Second Line of Defense Operates when pathogens penetrate the skin or mucous membranes Composed of cells, antimicrobial chemicals, and processes Many of these components are contained or originate in the blood

15 The Body's Second Line of Defense Defense Components of Blood Plasma Mostly water containing electrolytes, dissolved gases, nutrients, and proteins Serum is the fluid remaining when clotting factors are removed Contains iron-binding compounds Iron needed for metabolism Some microbes produce proteins that bind iron Complement proteins and antibodies are also found in plasma

16 The Body's Second Line of Defense Defense Components of Blood Defensive blood cells: leukocytes Cells and cell fragments in plasma called formed elements Three types of formed elements Erythrocytes Carry oxygen and carbon dioxide in the blood Platelets Involved in blood clotting Leukocytes Involved in defending the body against invaders Divided into granulocytes and agranulocytes

17 Figure 15.4 A schematic representation of hematopoiesis. Blood stem cell in bone marrow Erythroid stem cell Myeloid stem cell Lymphoid stem cell Erythrocyte Platelets Basophil Neutrophil Eosinophil Monocyte Lymphocyte Clotting, inflammation Inflammation Phagocytosis Gas transportation Innate immunity, second line of defense Leukocytes Adaptive immunity

18 Figure 15.5 Leukocytes as seen in stained blood smears. Basophil 0.5 1% Basophils stain blue with basic dye methylene blue Eosinophils stain red/orange with acidic dye eosin Neutrophils stain lilac with mix of acidic and basic dyes Granulocytes Eosinophil 2 4% Lymphocyte 20 25% Agranulocytes Neutrophil 60 70% Monocyte 3 8%

19 Figure 15.6 The events in phagocytosis. 1 Chemotaxis of phagocyte to microbes Microbes Pseudopods move (chemotaxis) 2 Adherence 3 Ingestion of microbes by phagocytes Phagosome 4 Fusion of a series of vessicles, including lysosomes Golgi body Lysosome Nucleus 5 Killing of microbes by enzymes and other chemicals Phagolysosome Residual body Pseudopod Phagocyte 6 Elimination (exocytosis)

20 The Body's Second Line of Defense Nonphagocytic Killing Killing by eosinophils Attack parasitic helminths by attaching to their surface Secrete toxins that weaken or kill the helminth Eosinophilia is often indicative of a helminth infestation or allergies Eosinophil mitochondrial DNA and proteins form structure that kills some bacteria

21 The Body's Second Line of Defense Nonphagocytic Killing Killing by natural killer lymphocytes Secrete toxins onto surface of virally infected cells and tumors Differentiate normal body cells because they have membrane proteins similar to the NK cells

22 The Body's Second Line of Defense Nonphagocytic Killing Killing by neutrophils Can destroy microbes without phagocytosis Produce chemicals that kill nearby invaders Generate extracellular fibers called neutrophil extracellular traps (NETs) that bind to and kill bacteria

23 The Body's Second Line of Defense Nonspecific Chemical Defenses Against Pathogens Toll-like receptors (TLRs) Integral membrane proteins produced by phagocytic cells Bind pathogen-associated molecular patterns (PAMPs) Initiate defensive responses Apoptosis Secretion of inflammatory mediators Stimulate adaptive immune response

24 The Body's Second Line of Defense Nonspecific Chemical Defenses Against Pathogens NOD proteins-nucleotide-binding oligomerization domain-like receptors, in short NOD-like receptors (NLRs) Cytosolic proteins that bind PAMPs Trigger inflammation, apoptosis, and other innate responses Mechanism of action still being researched

25 The Body's Second Line of Defense Nonspecific Chemical Defenses Against Pathogens Interferons Protein molecules released by host cells to nonspecifically inhibit the spread of viral infections Cause many symptoms associated with viral infections Two types Types I (alpha and beta) Type II (gamma)

26 Figure 15.7 The actions of alpha and beta interferons. 1 Virus infects cell. Virus Doublestranded RNA IFN gene Nucleus 2 Viral replication in cell triggers transcription and translation of IFN- or IFN-, depending on type of host cell. Time passes 5 Meanwhile, the infected cell dies, releasing viruses. mrna IFN Infected cell 3 Interferon is released, diffuses to neighboring uninfected cells, and binds to receptors. Infected cell at a later time Interferon receptor mrna Uninfected neighboring cell Inactive AVPs AVP gene 4 Binding triggers transcription and translation of inactive antiviral proteins (AVPs). Time passes Inactive AVP Doublestranded viral RNA Active AVPs Ribosome Same neighboring cell now protected at the later time mrna 6 When the second cell becomes infected with viruses, doublestranded RNA of the virus activates AVP. 7 Active AVPs degrade mrna and bind to ribosomes, which stops protein synthesis and viral replication.

27 The Body's Second Line of Defense Nonspecific Chemical Defenses Against Pathogens Complement Set of serum proteins designated numerically according to their order of discovery Complement activation results in lysis of the foreign cell Indirectly trigger inflammation and fever Complement can be activated in three ways Classical pathway Alternative pathway Lectin pathway

28 Figure 15.8 Pathways by which complement is activated. Classical pathway Alternative pathway Antigen C3b Endotoxin and glycoproteins Lectin pathway Mannose Lectins Antibody C3b Factors B, D, and P Complement proteins 1, 2, 4 Complement cascade Activation (C3 C3a + C3b) Opsonization Inflammation C5 convertases C5 C5a + C5b Inflammation Membrane attack complex and cell lysis

29 Figure 15.9 The classical pathway and complement cascade. H 2 O C1 1 H 2 O H 2 O C1 becomes an active enzyme when it binds to antibody-antigen complexes. C2 C4 C4 C2 C3 2 Pathogen Enzymatic C1 Enzyme C1 splits molecules of C2 and of C4. 3 Antigen Antibody Fragments of C2 and C4 combine to form a second enzyme that splits C3 into C3a and C3b. Membrane attack complex Causes chemotaxis of phagocytes and triggers inflammation Causes inflammation C9 C9 C5a C9 C9 C9 C9 C9 C9 C9 C9 C8 C7 C5b C6 C5b C4b C4b C2b C3b C2a C2a C2b C2b C4a C4b Enzyme C4b 4 Enzyme C3b combines with the remaining fragments of C2 and C4 to form a third enzyme. C3a C3b 6 5 Cytoplasmic membrane H 2 O C5b combines with C6, C7, C8, and several molecules of C9 to form a membrane attack complex (MAC). A MAC drills a circular hole in the pathogen s cytoplasmic membrane, leading to lysis of the cell. This enzyme cleaves C5 into C5a and C5b. C5 C3 Causes chemotaxis of phagocytes and triggers inflammation C3a C3b Acts as opsonin

30 The Body's Second Line of Defense Inflammation Nonspecific response to tissue damage from various causes Characterized by redness, heat, swelling, and pain Two types Acute Chronic

31 The Body's Second Line of Defense Inflammation Acute inflammation Develops quickly and is short lived Is typically beneficial Is important in the second line of defense Dilation and increased permeability of the blood vessels Migration of phagocytes Tissue repair Chronic inflammation Long-lasting Damage to tissues can cause disease

32 Figure The stimulation of inflammation by complement. C3a C5a C3a C5a Granule containing chemicals Inflammatory mediators

33 Figure The dilating effect of inflammatory mediators on small blood vessels. Capillaries Mediator Dilated capillaries Blood flow Venule Blood flow Arteriole Before After

34 Figure Increased vascular permeability during inflammation. Normal permeability of venule Increased permeability of venule during inflammation Venule wall Small amount of fluid Interstitial spaces More fluid and antimicrobial chemicals Monocyte Small amount of fluid Monocyte squeezing through interstitial space (diapedesis) More fluid

35 Figure An overview of the events in inflammation following a cut and infection. Bacteria 1 2 A cut penetrates the epidermis barrier, and bacteria invade. Damaged cells release prostaglandins, leukotrienes, and histamine (shown in green here). 3 4 Prostaglandins and leukotrienes make vessels more permeable. Histamine causes vasodilation, increasing blood flow to the site. Macrophages and neutrophils squeeze through walls of blood vessels (diapedesis). Swelling Heat 5 Increased permeability allows antimicrobial chemicals and clotting proteins to seep into damaged tissue but also results in swelling, pressure on nerve endings, and pain Blood clot forms. More phagocytes migrate to the site and devour bacteria. Accumulation of damaged tissue and leukocytes forms pus. Nerve ending 9 Undifferentiated stem cells repair the damaged tissue. Blood clot is absorbed or falls off as a scab.

36 The Body's Second Line of Defense Fever A body temperature over 37 C Results when pyrogens trigger the hypothalamus to increase the body's core temperature Various types of pyrogens Bacterial toxins Cytoplasmic contents of bacteria released by lysis Antibody-antigen complexes Pyrogens released by phagocytes that have phagocytized bacteria Exact mechanism of fever is not known

37 Figure One theoretical explanation for the production of fever in response to infection. Hypothalamus 2 Hypothalamus secretes prostaglandin, which resets hypothalamic thermostat. 1 Chemicals secreted by phagocytes travel in blood to hypothalamus. 3 Nerve impulses cause shivering, higher metabolic rate, inhibition of sweating, and vasoconstriction. Wound 4 These processes increase body temperature to the point set by the hypothalamic thermostat.

38 The Body's Second Line of Defense Fever Continues as long as pyrogens are present Outcomes of fever Enhances effects of interferons Inhibits growth of some microbes May enhance the activities of phagocytes, cells of specific immunity, and the process of tissue repair

39 CHAPTER 16 Adaptive Immunity

40 Overview of Adaptive Immunity Adaptive immunity is the body's ability to recognize and defend itself against distinct invaders and their products Five attributes of adaptive immunity Specificity Inducibility Clonality Unresponsiveness to self Memory

41 Overview of Adaptive Immunity Involves activity of lymphocytes Two main types of lymphocytes B lymphocytes (B cells) Mature in the bone marrow T lymphocytes (T cells) Mature in the thymus Two types of adaptive immune responses Cell-mediated immune responses Antibody immune responses

42 Cell-Mediated Immunity: Overview

43 Elements of Adaptive Immunity The Tissues and Organs of the Lymphatic System Composed of lymphatic vessels and lymphatic cells, tissues, and organs Screen the tissues of the body for foreign antigens

44 Figure 16.2 The lymphatic system. Blood capillary From heart Tissue cell Tonsils Cervical lymph node Intercellular fluid Lymphatic ducts Thymus gland Lymph to heart via lymphatic vessels Gap in wall Axillary lymph node Heart Breast lymphatics Spleen Valve Abdominal lymph node To heart Lymphatic capillary Intestines Peyer s patches in intestinal wall Appendix Part of mucosaassociated lymphoid tissue (MALT) Cortex Afferent lymphatic vessel Medulla Red bone marrow Inguinal lymph node Lymphatic vessel Vein Valve (prevents backflow) Artery Lymphatic nodule Efferent lymphatic vessel Capsule Primary follicle

45 Elements of Adaptive Immunity The Tissues and Organs of the Lymphatic System Lymphoid organs Primary lymphoid organs Red bone marrow Thymus Secondary lymphoid organs Lymph nodes Spleen Tonsils Mucosa-associated lymphoid tissue (MALT)

46 Elements of Adaptive Immunity Antigens Properties of antigens Molecules the body recognizes as foreign and worthy of attack Recognized by three-dimensional regions called epitopes on antigens Large foreign macromolecules make the best antigens Include various bacterial components as well as proteins of viruses, fungi, and protozoa Food and dust can also contain antigenic particles

47 Figure 16.3a Antigens, molecules that provoke a specific immune response. Epitopes (antigenic determinants) Nucleus Cytoplasmic membrane Antigen Cytoplasm Epitopes (antigenic determinants)

48 Figure 16.3b-d Antigens, molecules that provoke a specific immune response. Extracellular microbes Endogenous antigens Autoantigens (normal cell antigens) Intracellular virus Exogenous antigens Virally infected cell Normal (uninfected) cell Exogenous antigens Endogenous antigens Autoantigens

49 Elements of Adaptive Immunity B Lymphocytes (B Cells) and Antibodies Found primarily in the spleen, lymph nodes, and MALT Small percentage of B cells circulate in the blood Major function is the secretion of antibodies

50 Elements of Adaptive Immunity B Lymphocytes (B Cells) and Antibodies Specificity of the B cell receptor (BCR) Each B lymphocyte has multiple copies of the B cell receptor Each B cell generates a single BCR Two variable regions of the BCR form the antigen-binding sites Each BCR recognizes only one epitope The entire repertoire of an individual's BCRs is capable of recognizing millions of different epitopes

51 Figure 16.4 B cell receptor (BCR). Heavy chain Light chain Epitope Antigenbinding sites Variable region Disulfide bond Transmembrane portion of BCR Cytoplasmic membrane of B lymphocyte Cytoplasm

52 Elements of Adaptive Immunity B Lymphocytes (B Cells) and Antibodies Specificity and antibody structure Antibodies are immunoglobulins similar to BCRs Secreted by activated B cells called plasma cells Have antigen-binding sites and antigen specificity identical to the BCR of the activated B cell

53 Figure 16.5 Basic antibody structure. Arm (F ab ) Light chain Arm (F ab ) Antigen-binding sites Variable region of heavy chain Variable region of light chain Hinge Hinge Stem (F c ) Constant region of light chain Constant region of heavy chain Stem (F c ) Heavy chains

54 Elements of Adaptive Immunity B Lymphocytes (B Cells) and Antibodies Antibody function Antigen-binding sites are complementary to epitopes Antibodies function in several ways Activation of complement and inflammation Neutralization Opsonization Killing by oxidation Agglutination Antibody-dependent cellular cytotoxicity (ADCC)

55 Figure 16.6 Five functions of antibodies. Adhesin proteins Bacterium Toxin Virus Neutralization Agglutination NK lymphocyte Opsonization F c receptor protein Pseudopod of phagocyte F c receptor protein Perforin allows granzyme to enter, triggers apoptosis and lysis Antibody-dependent cellular cytotoxicity (ADCC) Bacteria die Oxidation

56 Humoral Immunity: Antibody Function

57 Elements of Adaptive Immunity B Lymphocytes (B Cells) and Antibodies Classes of antibodies Threats confronting the immune system are variable Antibody class involved in the immune response varies Type of antigen Portal of entry Antibody function needed Five different classes of antibodies

58 Elements of Adaptive Immunity B Lymphocytes (B Cells) and Antibodies Classes of antibodies IgM first antibody produced IgG most common and longest-lasting antibody IgA associated with body secretions IgE involved in response to parasitic infections and allergies IgD exact function is not known

59 Humoral Immunity: Antibody Function

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61 Elements of Adaptive Immunity T Lymphocytes (T Cells) Produced in the red bone marrow and mature in the thymus Circulate in the lymph and blood Migrate to the lymph nodes, spleen, and Peyer's patches Have T cell receptors (TCRs) on their cytoplasmic membrane

62 Elements of Adaptive Immunity T Lymphocytes Specificity of the T cell receptor (TCR) TCRs do not recognize epitopes directly TCRs only bind epitopes associated with an MHC protein T cells act primarily against cells that harbor intracellular pathogens Some T cells act against body cells that produce abnormal cell-surface proteins

63 Figure 16.7 A T cell receptor (TCR). Variable regions Constant regions Antigen-binding site Carbohydrate Cytoplasmic membrane of T cell T cell receptor (TCR) Cytoplasm

64 Elements of Adaptive Immunity T Lymphocytes Types of T lymphocytes Based on surface glycoproteins and characteristic functions, three types Cytotoxic T lymphocyte Directly kills other cells Helper T lymphocyte Helps regulate B cells and cytotoxic T cells Includes type 1 and type 2 helper T cells Regulatory T lymphocyte Represses adaptive immune responses

65 Elements of Adaptive Immunity Clonal Deletion Vital that immune responses not be directed against autoantigens Body eliminates self-reactive lymphocytes Lymphocytes that react to autoantigens undergo apoptosis

66 Figure 16.8 Clonal deletion of T cells. Stem cell (in red bone marrow) 1 Thymus T cells 2 TCRs with differently shaped binding sites MHC Epitope 3 Thymus Recognize MHC? Thymus cells cells No Yes Receive survival signal 4 Recognize MHC-autoantigen? Apoptosis No Few Yes Most Apoptosis Repertoire of immature Tc cells Regulatory T cell (Tr)

67 Figure 16.9 Clonal deletion of B cells. Stem cell (in red bone marrow) 1 B cells 2 Cell with autoantigens BCRs with 3 differently shaped binding sites 4 Cell with autoantigens Apoptosis Blood vessel To spleen

68 Elements of Adaptive Immunity Immune Response Cytokines Soluble regulatory proteins that act as intercellular signals Cytokines secreted by various leukocytes Cytokine network Complex web of signals among cells of the immune system

69 Elements of Adaptive Immunity Immune System Cytokines Interleukins (ILs) Signal among leukocytes Interferons (IFNs) Antiviral proteins that may act as cytokines Growth factors Proteins that stimulate stem cells to divide Tumor necrosis factor (TNF) Secreted by macrophages and T cells to kill tumor cells and regulate immune responses and inflammation Chemokines Chemotactic cytokines that signal leukocytes to move

70 Preparation for an Adaptive Immune Response The Roles of the Major Histocompatibility Complex and Antigen-Presenting Cells Group of antigens first identified in graft patients Important in determining compatibility of tissues for tissue grafting Major histocompatibility antigens are glycoproteins found in the membranes of most cells of vertebrate animals Hold and position antigenic determinants for presentation to T cells

71 Preparation for an Adaptive Immune Response The Roles of the Major Histocompatibility Complex Antigens bind in the antigen-binding groove of MHC molecules Two classes of MHC proteins MHC class I Present on all cells except red blood cells MHC class II Present on antigen-presenting cells (APCs) Include B cells, macrophages, and dendritic cells

72 Figure The two classes of major histocompatibility complex (MHC) proteins. Antigen-binding sites (grooves) Cytoplasmic membrane Class I MHC on every nucleated cell Class II MHC on B cell or other antigen-presenting cell (APC) Cytoplasm

73 Preparation for an Adaptive Immune Response Antigen Processing Antigens processed for MHC proteins to display epitopes Different processes for endogenous and exogenous antigens

74 Figure The processing of T-dependent endogenous antigens. 1 Polypeptide is catabolized. MHC I protein in membrane of endoplasmic reticulum Epitopes MHC I protein epitope complex 2 Lumen of endoplasmic reticulum Epitopes are loaded onto complementary MHC I proteins in the ER. 3 Golgi bodies package MHC I protein epitope complexes into vesicles. 4 Vesicles fuse with cytoplasmic membrane. MHC I protein epitope complexes on cell surface Cytoplasmic membrane 5 MHC I protein epitope complexes are displayed on cytoplasmic membranes of all nucleated cells.

75 Figure The processing of T-dependent exogenous antigens. Phagocytosis by APC Exogenous pathogen with antigens MHC II protein epitope complex 1 MHC II protein in membrane of vesicle Epitopes in phagolysosome 2 Vesicles fuse and epitopes bind to complementary MHC II molecules. 3 Vesicle fuses with cytoplasmic membrane. MHC II protein epitope complexes on cell surface Cytoplasmic membrane 4 MHC II protein epitope complexes are displayed on cytoplasmic membranes of antigenpresenting cell.

76 Cell-Mediated Immune Responses Respond to intracellular pathogens and abnormal body cells Common intracellular pathogens are viruses The response is also effective against cancer cells, intracellular protozoa, and intracellular bacteria

77 Cell-Mediated Immune Responses Activation of Cytotoxic T Cell Clones and Their Functions Adaptive immune responses initiated in lymphoid organs Steps involved in activation of cytotoxic T cells Antigen presentation Helper T cell differentiation Clonal expansion Self-stimulation

78 Figure Activation of a clone of cytotoxic T (Tc) cells. 1 Antigen presentation Dendritic cell MHC I MHC II Epitope TCR DC MHC I CD8 Epitope TCR 2 Th cell Th differentiation IL-2 IL-12 Inactive Tc cell IL-2 receptor (IL-2R) Tc cell Immunological synapse Th1 cell 3 Clonal expansion IL-2R Active Tc cells Memory T cell IL-2 IL-2 4 Self-stimulation IL-2R Active Tc cells IL-2

79 Figure 16.15a A cell-mediated immune response. Active cytotoxic T (Tc) cell TCR CD8 Viral epitope MHC I protein Virally infected cell Intracellular virus

80 Figure 16.15b-c A cell-mediated immune response. Tc cell Perforin Granzyme Tc cell Inactive apoptotic enzymes Perforin complex (pore) Granzymes activate apoptotic enzymes Active enzymes induce apoptosis Inactive apoptotic enzymes CD95L CD95 Enzymatic portion of CD95 becomes active Active enzymes induceapoptosis Virally infected cell Virally infected cell

81 Cell-Mediated Immune Responses Memory T Cells Some activated T cells become memory T cells Persist for months or years in lymphoid tissues Immediately functional upon subsequent contacts with epitope-mhc complex specific to its TCR Memory response is more effective than the primary response

82 Cell-Mediated Immune Responses T Cell Regulation Regulation needed to prevent T cell response to autoantigens T cells require additional signals from an antigenpresenting cell Interaction of the T cell and antigen-presenting cell stimulates the T cell to respond to the antigen Regulatory T cells also moderate cytotoxic T cell activity

83 Antibody Immune Responses Antibody immune responses mounted against exogenous pathogens Activates only in response to specific pathogens

84 Figure The effects of the binding of a T-independent antigen by a B cell. BCRs Polysaccharide with repeating subunits B cell Plasma cells Antibodies

85 Figure A T-dependent antibody immune response. Repertoire of Th cells (CD4 cells) Th cell CD4 TCR Epitope CD4 CD28 TCRs 1 APC presents antigen to Th cells for Th activation and cloning. APC MHC II APC CD80 (or CD86) Th cell clones IL-4 2 Th cell differentiates into Th2 cell. CCR3 CCR4 Th2 cell MHC II proteins Th2 cell Th2 cell TCR Epitope CD4 CD40L Repertoire of B cells IL-4 MHC II B cell CD40 3 Th2 cell activates B cell. Clone of plasma cells 4 Antibodies Memory B cells

86 Humoral Immune Responses Inducement of T-Dependent Humoral Immunity Plasma cells Majority of cells produced during B cell proliferation Only secrete antibody molecules complementary to the specific antigen Short-lived cells that die within a few days of activation Their antibodies and progeny can persist

87 Humoral Immune Responses Memory B Cells and the Establishment of Immunological Memory Produced by B cell proliferation but do not secrete antibodies Have BCRs complementary to the epitope that triggered their production Long-lived cells that persist in the lymphoid tissue Initiates antibody production if antigen is encountered again

88 Figure The production of primary and secondary antibody immune responses.

89 Types of Acquired Immunity Specific immunity acquired during an individual's life Two types Naturally acquired Response against antigens encountered in daily life Artificially acquired Response to antigens introduced via a vaccine Distinguished as either active or passive

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