Target cell lysis Opsonization Activation of the inflammatory response (e.g. degranulation, extravasation) Clearance of immune complexes
|
|
- Lorraine Edwards
- 6 years ago
- Views:
Transcription
1 Immunology Dr. John J. Haddad Chapter 13 Complement Major roles of complement (Figure 13-1): Target cell lysis Opsonization Activation of the inflammatory response (e.g. degranulation, extravasation) Clearance of immune complexes There are three major pathways of complement activation (sometimes called complement fixation ): Classical pathway involves antibodies Alternative pathway no antibody is required Lectin pathway similar to the classical pathway in most of its components, but it is initiated by mannosebinding lectin (MBL), an acute phase protein made in response to microbial infection. The MBL binds to mannose on microbial surfaces. All three pathways can generate a membrane attack complex (MAC) that inserts into membranes of cells, susceptible bacteria and enveloped viruses and makes them osmotically unstable, resulting in lysis. They all also generate small diffusible reaction products that induce local vasodilation and chemotaxis of phagocytic cells, resulting in inflammation. They all also enhance phagocytosis by binding to complement receptors on phagocytic cells. Complement proteins are synthesized and secreted by liver hepatocytes, blood monocytes, tissue macrophages, and epithelial cells of the gastrointestinal and genitourinary tracts. Many of the complement components are proenzymes that have their active sites masked. Activation occurs by proteolytic cleavage, resulting in removal of the mask and exposure of the active site. Each of the pathways involve a cascade of proteolytic steps. By convention, an activated enzyme in a complement pathway is indicated with a bar drawn over it. Note: In learning and studying the complement pathways, focus heavily on Figure 13-2 in the text, and know your way around this figure. The pictures shown in Figures 13-3 and 13-5 may help you picture what is going on, but they are cartoons. You should understand complement activation by knowing the names of the components and the roles they play in the respective pathways. Classical pathway of complement activation The classical pathway begins with antibody binding to a surface. IgM is the best activator, but the IgG1, IgG2 and IgG3 isotypes also can activate complement. IgM does it best because it is a pentamer of four-chain units and therefore contains five Fc regions in close proximity. The first component of the classical pathway, C1, crosslinks Fc fragments. For IgG to activate complement, independent IgG molecules must bind to the surface no more than nanometers apart to allow crosslinking by C1q. One IgM molecule is enough to allow complement to lyse a red blood cell, whereas about 1,000 IgG molecules are required. C1q is associated with C1r and C1s. Binding of C1q to immunoglobulin causes a conformational change in C1r to autocatalytically activate itself to C1r-bar. C1r-bar then activates C1s to C1s-bar, which then cleaves C4 (to C4a and C4b). C4b covalently binds to a cell surface near C1q by an amide linkage, and C4a diffuses away. 63
2 C2 binds to C4b, and then is cleaved by C2s-bar to C2a (which remains associated with C4b) and C2a which diffuses away. C4b2a-bar is called the classical C3 convertase, and its activity is to cleave C3 into C3b and C3a. The C3 convertase catalyzes the amplification step in complement activation, since one C3 convertase complex can cleave more than 200 C3 molecules. When C3 is cleaved, a thioester bond becomes labile and reactive carbonyl group on C3b reacts with hydroxyl or amino groups on the cell surface. Thus many C3b molecules become covalently bound to the cell surface. The C3a fragment diffuses away. Some C3b molecules associate with C4b2a to form C4b2a3b-(bar), the classical C5 convertase, which cleaves C5 into C5b, which attaches to the cell surface, and C5a which diffuses away. Cleavage of C5 is the last proteolytic step in the classical pathway. The C5b fragment initiates the assembly of the membrane attack complex (MAC) to be discussed a bit later. Alternative pathway of complement activation The alternative pathway can also generate the C5b protein by a pathway involving four proteins: C3, factor B, factor D and properdin. It does not involve antibody. Both gram-negative and gram-positive microorganisms, as well as some other foreign substances and organisms (Table 13-3), can activate complement by the alternative pathway. The unstable thioester bond of C3 (referred to above) can spontaneously hydrolyze at a low frequency to form C3b and C3a, and the C3b can attach covalently to the bacterial or mammalian cell surface. The sialic acid present on mammalian cell surface glycoproteins generally inactivates C3b that binds to mammalian cell surfaces. However, bacteria do not have sialic acid, and the C3b remains active long enough to bind factor B in the presence of Mg +2 ion. Factor D then cleaves factor B, and Bb remains in a complex with C3b (C3bBb-bar) while the Ba fragment diffuses away. C3bBb-bar has C3 convertase activity, and it is referred to as the alternative pathway C3 convertase. C3bBb-bar is unstable and has a half-life of only 5 minutes unless properdin binds and stabilizes it. The stabilized complex has a half-life of 30 minutes. As in the classical pathway, the C3 convertase catalyzes the amplification step, cleaving as many as 200 C3 molecules. As many as 2 x 10 6 generated in 5 minutes. Many attach covalently to the surface on which the complement was activated (see above). Some associate with C3bBb to form C3bBb3b(bar) the alternative pathway C5 convertase. Like the classical C5 convertase, C4b2a3b(bar), it cleaves C5 to generate C5b which inserts into membranes to start forming the MAC complex, and C5a that diffuses away. Lectin pathway of complement activation The mannose-binding lectin, MBL, is an acute phase protein that is produced upon microbial infection. It binds to mannose on the surface of microorganisms, and a protease associated with MBL, MASP (for MBL-associated protease) that resembles C1qr, cleaves C4 and C2 to generate C4b2a(bar), the classical C3 convertase. From there on, it is just like the classical pathway. Formation of the MAC complex C5b is very labile, and is inactivated within 2 minutes unless it is stabilized by binding of C6 (Figure 13-5, panels e and f). As C5b6 binds C7 to form C5b67, it undergoes a conformational change that exposes hybrophobic regions that enable it to insert into the phospholipid membrane if activation occurred on a cell. Subsequent binding of C8 generates C5b678 which makes a small pore, or channel, through the membrane approximately 10 angstroms in diameter. Subsequent binding and polymerization of molecules of C9 generates a much larger pore angstroms in diameter. Ions and small molecules diffuse freely, and cell undergoes osmotic lysis, 64
3 If C5b67 is generated on an immune complex that does not sit on a membrane, it is released into the medium. If it encounters a nearby cell before decaying (i.e., becoming inactive) it can insert there and cause bystander lysis by building a MAC on the nearby uninvolved cell. This can contribute to some disease processes. 65
4 Regulation of the complement system The action of complement much be confine to designated targets because once activated, complement s activity is non-specific. Many of the proteins that regulate complement are described in Table One intrinsic aspect that contributes to regulation is the inherent instability of intermediary components. For example, C3b s site for attachment to membranes becomes inactive by the time it diffuses 40 nm away from the C3 convertase that generated it. 2. Inhibitory proteins exist. For example, C1InH form as a complex with C1r2s2 and promotes its dissociation from C1q. Inhibits classical pathway. 3. There is a whole family of C3 convertase regulators. This is an important step at which to regulate complement since it prevents the major amplification step. The regulatory proteins consist of a number of structurally-related proteins containing short consensus repeats (CSRs) of amino acids. They are encoded by closely-linked genes in the regulators of complement activation (RCA) locus on human chromosome 1. The pathways of action of several of these are illustrated in Figure Several of these prevent assembly of the classical C3 convertase by binding to C4b ((C4bBP, CR1, MCP)) and preventing attachment of C2a. In the alternative pathway, regulatory components bind to C3b (CR1, MCP or factor H) and prevent attachment of B. The C4b or C3b is then inactivated by cleavage by the serum protease, factor I. Several regulatory components cause dissociation the enzymatically-active component (C2a or Bb) from the classical or alternative pathway C3 convertase, respectively. C4bBP, CR1, factor H and decay-accelerating factor (DAF) all have this activity. Once dissociated, the cell-bound component (C4b or C3b) is inactivated by cleavage by factor I. Interestingly, the mechanism of generation of C3d, the component that binds to CR2 (CD21) that makes up art of the B cell coreceptor (see Chapter 11, Figure 11-9) is described in Figure Complement activity is also regulated at the level of the MAC. Your own cells are generally resistant to lysis by your own or any human complement due to two proteins present on the membrane of many cell types homologous restriction factor (HRF) and membrane inhibitor of reactive lysis (MIRL, or CD59). These bind to C8 and prevent assembly and membrane insertion of C9. Interestingly, transplantation of an organ from a different species (a xenogeneic organ) into a human results in very fast rejection (called hyperacute rejection) of the organ, largely because of complement activation and the inability of the xenogeneic HRF and MIRL to inactivate human complement. Studies are being done in which pig HRF and MIRL are being genetically replaced by human HRF and MIRL. Studies in monkeys suggest that this approach may protect a transplanted xenogeneic organ from hyperacute rejection. Biological consequences of complement activation These are summarized in Table Antibody and complement play a major role in lysis of membrane-coated particles or cells by means of the MAC. Susceptible targets include enveloped viruses (e.g., retroviruses like HIV) and many gramnegative bacteria. Some gram-negative bacteria escape lysis by fabricating a smooth coat that is resistant to MAC insertion. Gram-positive bacteria are generally resistant to MAC insertion due to a thick peptidoglycan cell wall layer or capsule. Streptoccus pneumoniae can activate complement, but C3b cannot covalently attach to it because of its capsule. 66
5 Other organisms produce proteins that mimic the effect of normal complement regulatory components such as C4bBP, CR1 and DAF, thereby protecting themselves from lysis. Many nucleated cells, including most cancer cells, can endocytose the MAC, thereby preventing osmotic disruption and death by osmotic lysis. 2. Complement opsonizes immune complexes, or makes them highly susceptible to phagocytosis. The C3b or C4b bound to the immune complexes or particle surfaces binds to complement receptors C1, C3 and C4. They are then phagocytosed. Some degradation products also bind (e.g., ic3b). The C5a product of C5 cleavage increases the number of CR1 molecules on the neutrophil surface ten-fold from 5,000 to 50,000, thereby facilitating phagocytosis. 3. Complement participates in virus neutralization by coating the virus and preventing attachment and subsequent infection of cells. Coated viruses also can be bound by complement receptors on inflammatory cells including neutrophils and macrophages, and this leads to their destruction by phagocytosis or by release of toxic mediators. 4. Complement facilitates clearance of immune complexes from the body. Deficiency in complement components that comprise C1, C2 or C4 can predispose a person to the autoimmune disease, lupus erythematosis. This is because when autoimmune complexes are formed, the classical pathway cannot generate C3b to opsonize the complexes. Deficiency in complement receptor 1 (CR1) which binds C3b also predisposes to lupus. This is because the CR1 on the surface of red blood cells (RBCs) participated in clearing immune complexes from the body. There are only about 100 CR1 molecules on each RBC surface, but there are so many RBCs, they can carry a lot of immune complexes. These complexes are stripped from the RBCs in the liver and spleen, and the complexes are phagosytosed and destroyed (Figure 13-14). 5. Complement plays a major role in the inflammatory response. When we described the steps in complement activation, we referred to C3a, C4a and C5ab as fragments that diffused away and did not participate in the complexes that were forming. These components are potent mediators called anaphylatoxins that bind to receptors on mast cells and basophils and stimulate release of histamine. C5a is the most powerful of the anaphylatoxins and is active at concentrations as low as M. Histamine has potent effects, increasing vascular permeability and stimulating smooth muscle contraction. C3a, C5a and C5b67 all contribute to inflammation by inducing extravasation of monocytes and neutrophils. Deficiencies in complement components or in regulators of complement can cause a number of serious diseases or susceptibilities C3 deficiencies are the most severe. Without C3, the MAC cannot be activated. Other deficiencies make a person susceptible to specific problems. For example, factor D or properdin deficiencies are associated with recurrent Neisseria infections. Deficiency of C1Inh, which occurs in 1 of 1000 people as an autosomal dominant, gives rise to hereditary angioedema. Deficiency of DAF or HRF due to a defective glycosyl phosphatidylinositol membrane anchor can lead to inability to inactivate MACs that may insert into a patient s own cells. RBCs can be lysed, resulting in paroxysmal nocturnal hemoglobinurea (hemoglobin in the patient s urine) due to chronic hemolytic anemia. 67
History. Chapter 13. Complement Components. Complement Pathways
History Chapter 13 Complement Jules Border in 1890 s discovered complement Paul Ehrlich coined the term complement The activity of blood serum that completes the action of antibody Now: Set of serum proteins
More informationComplement. History. Chapter 7. Complement Components. Complement Pathways. Pathways of complement activation
History Chapter 7 Complement Jules Border in 1890 s discovered complement Paul Ehrlich coined the term complement The activity of blood serum that completes the action of antibody Now: Set of serum proteins
More informationHistory. Chapter 13. Complement Components. Complement Pathways
History Chapter 13 Complement Jules Border in 1890 s discovered complement Paul Ehrlich coined the term complement The activity of blood serum that completes the action of antibody Now: Set of serum proteins
More informationTopic (6): The Complement System
Topic (6): The Complement System Introduction The complement system is a complex system of many different glycoproteins. It comprises several plasma proteins that sequentially activate each other by proteolytic
More informationTHE COMPLEMENT SYSTEM OBJECTIVES:
Dr Mohammed Al- ani THE COMPLEMENT SYSTEM OBJECTIVES: When you finish this section, you should be able to: 1. Describe the effects of complement activation. 2. Outline the Classical, Mannan-Binding (MB)
More informationSuvasini Modi Complement System Activation of Membrane attacking complex (MAC) and its effect and regulation
Figure- 1 https://en.wikipedia.org/wiki/complement_system Suvasini Modi Complement System Activation of Membrane attacking complex (MAC) and its effect and regulation Content Introduction Activation of
More informationComplement: History. Discovered in 1894 by Bordet. It represents lytic activity of fresh serum
Complement: History Discovered in 1894 by Bordet It represents lytic activity of fresh serum Its lytic activity destroyed when heated at 56C for 30 min Complement functions Host benefit: opsonization to
More informationCD B T NK NKT!! 1
CD B T NK NKT!! 1 2 !! 3 4 5 6 7 8 9 10 11 Biological effects of C5a 12 13 Opsonization and phagocytosis 14 15 http://www.med.sc.edu:85/book/wel come.htm 16 http://www.med.sc.edu:85/book/im munol-sta.htm
More informationTHE COMPLEMENT SYSTEM OBJECTIVES:
THE COMPLEMENT SYSTEM OBJECTIVES: When you finish this section, you should be able to: 1. Describe the effects of complement activation. 2. Outline the Classical, Mannan-Binding (MB) Lectin and Alternative
More informationIntroduction. A system of soluble enzymes and proteins. Complement components: C1 to C9, B, D and P
Complement Introduction A system of soluble enzymes and proteins Complement components: C1 to C9, B, D and P When activated, each component is split into small and large (major) fragments a b *A horizontal
More informationThe term complement refers to the ability of a system of some nonspecific proteins in normal human serum to complement, i.e., augment the effects of
COMPLEMENT SYSTEM The term complement refers to the ability of a system of some nonspecific proteins in normal human serum to complement, i.e., augment the effects of other components of immune system,
More informationاالستاذ المساعد الدكتور خالد ياسين الزاملي \مناعة \المرحلة الثانية \ التحليالت المرضية \ المعهد التقني كوت
Complement System The term complement refers to the ability of a system of some nonspecific proteins in normal human serum to complement, i.e., augment the effects of other components of immune system,
More informationComplement. Definition : series of heat-labile serum proteins. : serum and all tissue fluids except urine and CSF
Complement Complement Definition : series of heat-labile serum proteins Site : serum and all tissue fluids except urine and CSF Synthesis : in liver appear in fetal circulation during 1 st 13 W Function
More informationBasic Immunology. Lecture 16th. Complement system
Basic Immunology Lecture 16th Complement system Components: Inactive factors in the serum and body fluids which can activate each other in an enzyme cascade Cell surface receptors (CR) for binding the
More informationLecture 07. Complement
Lecture 07 Complement Science is a social process. It happens on a time scale longer than a human life. If I die, someone takes my place. You die; someone takes your place. What's important is to get it
More informationAttribution: University of Michigan Medical School, Department of Microbiology and Immunology
Attribution: University of Michigan Medical School, Department of Microbiology and Immunology License: Unless otherwise noted, this material is made available under the terms of the Creative Commons Attribution
More informationCellular & Molecular Immunology 2009
Cellular & Molecular Immunology 2009 Complement Nicholas M. Ponzio, Ph.D. Department of Pathology & Laboratory Medicine March 4, 2009 Innate and adaptive immunity FAMOUS BELGIANS Jules Jean Baptiste Vincent
More informationM1 - Immunology, Winter 2008
University of Michigan Deep Blue deepblue.lib.umich.edu 2008-09 M1 - Immunology, Winter 2008 Fantone, J.; Pietropaolo, M. T. Fantone, J., Pietropaolo, M. T. (2008, August 13). Immunology. Retrieved from
More informationInflammation. (4 of 5)
Inflammation (4 of 5) What will we discuss today? Plasma protein derived mediators Anti-inflammatory mediators Morphologic patterns of acute inflammation Plasma protein derived mediators 3 systems: -Complement
More informationCatalog Number: A114 Sizes Available: 250 µg/vial Concentration: 1.0 mg/ml (see Certificate of Analysis for actual concentration)
Name: C3b Catalog Number: A114 Sizes Available: 250 µg/vial Concentration: 1.0 mg/ml (see Certificate of Analysis for actual concentration) Form: Liquid Purity: >90% by SDS-PAGE Buffer: 10 mm sodium phosphate,
More informationThird 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 informationComplement pathways: Classical pathway Alternative pathway Lectin pathway
Complement Complement pathways: Classical pathway Alternative pathway Lectin pathway Complement proteins Classical pathway C1q C1r C1s C4 C2 Alternative pathway D C3 B Lectin pathway MBL MASP-1 MASP-2
More informationChapter 21: Innate and Adaptive Body Defenses
Chapter 21: Innate and Adaptive Body Defenses I. 2 main types of body defenses A. Innate (nonspecific) defense: not to a specific microorganism or substance B. Adaptive (specific) defense: immunity to
More informationComplement disorders and hereditary angioedema
Complement disorders and hereditary angioedema Michael M. Frank, MD Durham, NC The term complement was introduced more than 100 years ago to refer to a group of plasma factors important in host defense
More informationSecretory antibodies in the upper respiratory tract
Secretory antibodies in the upper respiratory tract B lymphocytes IgM (pneumococcus) Dimeric IgA J chain Polymeric immunoglobulin receptor (PigR) Polysaccharide capsule Epithelial cell Basolateral Secretory
More informationLecture 17: Attack by Complement and Counterattack by Microbes
Lecture 17: Attack by Complement and Counterattack by Microbes 2 Review Concepts of Complement Complement was addressed in Lecture 3 Major first line of defense (innate immunity) Major functions: Opsonization
More informationBiology of Fc γ Receptors. Selected Functions of Ig Isotypes
Biology of Fc γ Receptors Selected Functions of Ig Isotypes Biology of Fc γ Receptors 1 Functional Sites on the IgG Molecule V H V L C1q binding site FcγR binding site Glycosylation site Selected Functions
More informationComplement System. Jil Schrader 16 th of May 2018 Immunology Lecture
Source: https://bestprac.dk/2017/05/30/diagnosticering-af-almindelig-variabel-immundefekt-cvid-2/, letzter Zugriff: 14.05.2018 Complement System Jil Schrader 16 th of May 2018 Immunology Lecture Contents
More informationبسم هللا الرحمن الرحيم. Immunology lecture 7
بسم هللا الرحمن الرحيم Immunology lecture 7 Last time we studied the B cell receptor which is IgM & IgD. Today we will talk about the T Cell Receptor which is the TCR #TCR: it is the receptor that belongs
More informationMacrophage Activation & Cytokine Release. Dendritic Cells & Antigen Presentation. Neutrophils & Innate Defense
Macrophage Activation & Cytokine Release Dendritic Cells & Antigen Presentation Neutrophils & Innate Defense Neutrophils Polymorphonuclear cells (PMNs) are recruited to the site of infection where they
More informationInnate 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 informationNatural Defense Mechanisms
Color code: Important in red Extra in blue For team error adjustments, click here Natural Defense Mechanisms Objectives To know First (non-specific immunity) and second (adaptive immunity) lines of defense
More informationLECTURE: 21. Title IMMUNOGLOBULINS FUNCTIONS & THEIR RECEPTORS LEARNING OBJECTIVES:
LECTURE: 21 Title IMMUNOGLOBULINS FUNCTIONS & THEIR RECEPTORS LEARNING OBJECTIVES: The student should be able to: Determine predominant immunoglobulin isotypes in serum. Determine the predominant immunoglobulin
More informationThird line of Defense. Topic 8 Specific Immunity (adaptive) (18) 3 rd Line = Prophylaxis via Immunization!
Topic 8 Specific Immunity (adaptive) (18) Topics - 3 rd Line of Defense - B cells - T cells - Specific Immunities 1 3 rd Line = Prophylaxis via Immunization! (a) A painting of Edward Jenner depicts a cow
More informationCellular Pathology of immunological disorders
Cellular Pathology of immunological disorders SCBM344 Cellular and Molecular Pathology Witchuda Payuhakrit, Ph.D (Pathobiology) witchuda.pay@mahidol.ac.th Objectives Describe the etiology of immunological
More informationThe Biology of Fc γ Receptors and Complement
Discovery consists of seeing what everybody has seen, and thinking what nobody has thought --Albert Szent-György Nobel prize in Physiology or Medicine, 1937 The Biology of Fc γ Receptors and Complement
More informationChapter 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 informationTopics. 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 informationANTIBODIES Jiri Mestecky, M.D., Ph.D. - Lecturer
ANTIBODIES Jiri Mestecky, M.D., Ph.D. - Lecturer Distribution in body fluids: secretions plasma (serum), tears, saliva, milk, genitourinary, and intestinal Cells producing antibodies and their tissue distribution:
More informationComplement Elizabeth Repasky, PhD Fall, 2015
Complement Elizabeth Repasky, PhD Fall, 2015 Complement pathways: Classical pathway Alternative pathway Lectin pathway White Board Schematic C3 plays a central role in complement activation Complement
More informationMedical 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 informationThe Biology of Fc γ Receptors and Complement. Biology of Fc γ Receptors. Discovery consists of seeing what everybody
Discovery consists of seeing what everybody has seen, and thinking what nobody has thought The Biology of Fc γ Receptors and Complement --Albert Szent-György Nobel prize in Physiology or Medicine, 1937
More informationName: C3 Protein Concentrated Catalog Number: A113c Sizes Available: Concentration: Form: Activity: Purity: Buffer: Extinction Coeff.
Name: C3 Protein Concentrated Catalog Number: A113c Sizes Available: 1000 µg/vial Concentration: 5.0 mg/ml (see Certificate of Analysis for actual concentration) Form: Frozen liquid Activity: >70% versus
More informationClinical 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 informationComplement deficiencies, diagnosis and management. Contents
Complement deficiencies, diagnosis and management Classification: Protocol Lead Author: Dr Hana Alachkar Additional author(s): Victoria Blakeley Authors Division: Tertiary Medicine Unique ID: D5 Issue
More informationName: C5 Protein Catalog Number: A120 Sizes Available: Concentration: Form: Activity: Purity: Buffer: Extinction Coeff.
Name: C5 Protein Catalog Number: A120 Sizes Available: 250 µg/vial Concentration: 1.0 mg/ml (see Certificate of Analysis for actual concentration) Form: Frozen liquid Activity: >80% versus normal human
More informationLymphatic System. Where s your immunity idol?
Lymphatic System Where s your immunity idol? Functions of the Lymphatic System Fluid Balance Drains excess fluid from tissues Lymph contains solutes from plasma Fat Absorption Lymphatic system absorbs
More information10. Which of the following immune cell is unable to phagocytose (a) neutrophils (b) eosinophils (c) macrophages (d) T-cells (e) monocytes
Chapter 2. Acute and chronic inflammation(6): 1. In acute inflammation, which events occur in the correct chronological order? (Remembered from 2000, 2004 exam.) p50 (a) transient vasoconstriction, stasis
More information1. Overview of Innate Immunity
Chapter 15: Innate Immunity 1. Overview of Innate Immunity 2. Inflammation & Phagocytosis 3. Antimicrobial Substances 1. Overview of Innate Immunity Chapter Reading pp. 449-456 The Body s Defenses The
More informationINNATE IMMUNITY Non-Specific Immune Response. Physiology Unit 3
INNATE IMMUNITY Non-Specific Immune Response Physiology Unit 3 Protection Against Infection The body has several defenses to protect itself from getting an infection Skin Mucus membranes Serous membranes
More informationThe 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 informationImmunity. Chapter 38 Part 1
Immunity Chapter 38 Part 1 Impacts, Issues Frankie s Last Wish Infection with a common, sexually transmitted virus (HPV) causes most cervical cancers including the one that killed Frankie McCullogh 38.1
More informationThe Immune Response 2/21/2006 1
The Immune Response The reaction to any foreign substance (living or nonliving) regardless of pathologic consequences. Innate immunity (nonspecific) Acquired or adaptive immunity 2/21/2006 1 Innate Immunity
More informationIntroduction to the immune system Innate humoral immunity
Introduction to the immune system Innate humoral immunity Bartosz Wojciuk Immunology course for the 2nd year Medical Faculty students Pomeranian Medical University Academic year 2017/2018, winter semester
More informationInternal Defense Notes
Internal environment of animals provides attractive area for growth of bacteria, viruses, fungi Harm via: 1. destruction of cells 2. production of toxic chemicals To protect against foreign invaders, humans
More information2014 Pearson Education, Inc. Exposure to pathogens naturally activates the immune system. Takes days to be effective Pearson Education, Inc.
The innate immune interact with the adaptive immune system 1. Damage to skin causes bleeding = bradykinin activated, resulting in inflammation 2. Dendritic phagocytose pathogens Adaptive immunity 4. Dendritic
More information1. The barriers of the innate immune system to infection
Section 3.qxd 16/06/05 2:11 PM Page 12 12 SECTION THREE: Fleshed out 1. The barriers of the innate immune system to infection Questions What are the three characteristics of the innate immune system? What
More informationAll 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 informationNOTES: CH 43, part 2 Immunity; Immune Disruptions ( )
NOTES: CH 43, part 2 Immunity; Immune Disruptions (43.3-43.4) Activated B & T Lymphocytes produce: CELL-MEDIATED IMMUNE RESPONSE: involves specialized T cells destroying infected host cells HUMORAL IMMUNE
More informationPhysiology 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 informationمحاضرة 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 informationDiseases-causing agents, pathogens, can produce infections within the body.
BIO 212: ANATOMY & PHYSIOLOGY II 1 CHAPTER 16 Lecture: Dr. Lawrence G. Altman www.lawrencegaltman.com Some illustrations are courtesy of McGraw-Hill. LYMPHATIC and IMMUNE Systems Body Defenses Against
More informationFor questions 1-5, match the following with their correct descriptions. (24-39) A. Class I B. Class II C. Class III D. TH1 E. TH2
Questions Made by SI ATTENDEES!! :) Page 1 of 6 Student-Made Practice Exam Activity All questions, answers, and slide numbers are based off of Monday s SI activity, where students/attendees created possible
More informationAnastasios E. Germenis
Anastasios E. Germenis Professor and Chairman Department of Immunology & Histocompatibility School of Medicine University of Thessaly University Hospital of Larissa Greece agermen@med.uth.gr The Complement
More information1. 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 informationOverview 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 informationImmune 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 informationTime 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 informationBlood and Immune system Acquired Immunity
Blood and Immune system Acquired Immunity Immunity Acquired (Adaptive) Immunity Defensive mechanisms include : 1) Innate immunity (Natural or Non specific) 2) Acquired immunity (Adaptive or Specific) Cell-mediated
More informationImmunology Part II. Innate Immunity. 18. April 2018, Ruhr-Universität Bochum Marcus Peters,
Immunology Part II Innate Immunity 18. April 2018, Ruhr-Universität Bochum Marcus Peters, marcus.peters@rub.de Conserved structures of pathogens PAMPs are detected by Pattern Recognition Receptors PRRs
More informationM.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 informationUnderstanding the Complement Cascade and Its Role in Cold Agglutinin Disease. 1 M-CAgD-US-3006 February 2018
Understanding the Complement Cascade and Its Role in Cold Agglutinin Disease 1 February 2018 Instructions This information is provided as an educational resource for healthcare providers. It is not intended
More informationChapter 32. Non specific (Innate) Host Resistance ( 비특이적 ( 내재 ) 숙주방어 )
Chapter 32 Non specific (Innate) Host Resistance ( 비특이적 ( 내재 ) 숙주방어 ) Host Resistance Overview Immune system ( 면역계 ) Composed of widely distributed cells, tissues, and organs Recognizes foreign substances
More informationThe Complement System
Calbiochem The Complement System Complement Reagents of the Highest Quality The complement system provides innate defense against microbial infection and is a complement to antibody mediated immunity.
More informationResisting infection. Cellular Defenses: Leukocytes. Chapter 16: Innate host defenses Phagocytosis Lymph Inflammation Complement
Resisting infection Chapter 16: Innate host defenses Lymph Inflammation Complement Bio 139 Dr. Amy Rogers Innate defenses (ch. 16) Physical & chemical barriers; cellular defenses; inflammation, fever;
More informationCell-Derived Inflammatory Mediators
Cell-Derived Inflammatory Mediators Introduction about chemical mediators in inflammation Mediators may be Cellular mediators cell-produced or cell-secreted derived from circulating inactive precursors,
More information1. Lymphatic vessels recover about of the fluid filtered by capillaries. A. ~1% C. ~25% E. ~85% B. ~10% D. ~50%
BIOL2030 Huaman A&P II -- Exam 3 -- XXXX -- Form A Name: 1. Lymphatic vessels recover about of the fluid filtered by capillaries. A. ~1% C. ~25% E. ~85% B. ~10% D. ~50% 2. Special lymphatic vessels called
More informationThe 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 informationImmunology. Lecture- 8
Immunology Lecture- 8 Immunological Disorders Immunodeficiency Autoimmune Disease Hypersensitivities Immunodeficiency 1. Immunodeficiency --> abnormal production or function of immune cells, phagocytes,
More informationHypersensitivity is the term used when an immune response results in exaggerated or inappropriate reactions harmful to the host.
Hypersensitivity is the term used when an immune response results in exaggerated or inappropriate reactions harmful to the host. Hypersensitivity vs. allergy Hypersensitivity reactions require a pre-sensitized
More information16 Innate Immunity: M I C R O B I O L O G Y. Nonspecific Defenses of the Host. a n i n t r o d u c t i o n
ninth edition TORTORA FUNKE CASE M I C R O B I O L O G Y a n i n t r o d u c t i o n 16 Innate Immunity: Nonspecific Defenses of the Host PowerPoint Lecture Slide Presentation prepared by Christine L.
More informationSINGLE CHOICE. 5. The gamma invariant chain binds to this molecule during its intracytoplasmic transport. A TCR B BCR C MHC II D MHC I E FcγR
A Name: Group: SINGLE CHOICE 1. Which is the most important ligand of TLR5? A endospore B flagellin C polysaccharide capsule D DNA E pilus 2. The antibody-binding site is formed primarily by... A the constant
More informationThe Immune System is the Third Line of Defense Against Infection. Components of Human Immune System
Chapter 17: Specific Host Defenses: The Immune Response The Immune Response Immunity: Free from burden. Ability of an organism to recognize and defend itself against specific pathogens or antigens. Immune
More informationThe 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 informationInnate Immunity: Nonspecific Defenses of the Host
PowerPoint Lecture Presentations prepared by Bradley W. Christian, McLennan Community College C H A P T E R 16 Innate Immunity: Nonspecific Defenses of the Host Host Response to Disease Resistance- ability
More informationImmunobiology 7. The Humoral Immune Response
Janeway Murphy Travers Walport Immunobiology 7 Chapter 9 The Humoral Immune Response Copyright Garland Science 2008 Tim Worbs Institute of Immunology Hannover Medical School 1 The course of a typical antibody
More informationI. Defense Mechanisms Chapter 15
10/24/11 I. Defense Mechanisms Chapter 15 Immune System Lecture PowerPoint Copyright The McGraw-Hill Companies, Inc. Permission required for reproduction or display. Defense Mechanisms Protect against
More informationName: Factor H Catalog Number: A137 Sizes Available: Concentration: Form: Activity: Purity: Buffer: Extinction Coeff.: Molecular weight:
Name: Factor H Catalog Number: A137 Sizes Available: 250 µg/vial Concentration: 1.0 mg/ml (see Certificate of Analysis for actual concentration) Form: Frozen liquid Activity: >90% versus normal human serum
More informationJ07 Titer dynamics, complement fixation test and neutralization tests
avllm0421c (spring 2017) J07 Titer dynamics, complement fixation test and neutralization tests Outline titer, antibody titer dynamics complement, complement fixation reaction neutralization tests 2/35
More informationChapter 15 Adaptive, Specific Immunity and Immunization
Chapter 15 Adaptive, Specific Immunity and Immunization Adaptive Immunity: The third line of defense Third line of defense acquired and specific. Dual System of B and T lymphocytes- Immunocompetence Antigen
More informationChapter 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 informationImmunity. Innate & Adaptive
Immunity Innate & Adaptive Immunity Innate: response to attack is always the same Mechanical mechanisms Chemical mediators Cellular response Inflammatory response Adaptive: response to attack improves
More informationCHAPTER-VII IMMUNOLOGY R.KAVITHA, M.PHARM, LECTURER, DEPARTMENT OF PHARMACEUTICS, SRM COLLEGE OF PHARMACY, SRM UNIVERSITY, KATTANKULATHUR.
CHAPTER-VII IMMUNOLOGY R.KAVITHA, M.PHARM, LECTURER, DEPARTMENT OF PHARMACEUTICS, SRM COLLEGE OF PHARMACY, SRM UNIVERSITY, KATTANKULATHUR. The Immune Response Immunity: Free from burden. Ability of an
More informationAdaptive 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 informationA. Incorrect! The resistance that an individual acquires during life is known as specific immunity.
Microbiology - Problem Drill 13: Innate Immunity No. 1 of 10 1. Which type of immunity is attributed to the Anatomic, Physiologic, Phagocytic and inflammatory barriers? A. Specific Immunity B. Adaptive
More informationCELL 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 informationHow the Innate Immune System Profiles Pathogens
How the Innate Immune System Profiles Pathogens Receptors on macrophages, neutrophils, dendritic cells for bacteria and viruses Broad specificity - Two main groups of bacteria: gram positive, gram-negative
More informationTHE IMMUNE SYSTEM. There are specific defense mechanisms and nonspecific defense mechanisms also known as innate immune response.
Chapter 43 THE IMMUNE SYSTEM Disease-causing microorganisms are called pathogens. They include bacteria, viruses, protozoans and fungi. Immunology is the study of specific defense mechanisms. Two major
More information1) Mononuclear phagocytes : 2) Regarding acute inflammation : 3) The epithelioid cells of follicular granulomas are :
Pathology Second 1) Mononuclear phagocytes : - Are the predominant cells in three day old wounds - Are common in liver, spleen and pancreasd - Produce fibroblast growth factor - Secrete interferon-g -
More information