Biological Sciences
Humoral Immunity
Humoral immunity is a component of the immune system that involves the production of antibodies by B cells. These antibodies circulate in the blood and lymph, targeting pathogens such as bacteria and viruses. Humoral immunity plays a crucial role in defending the body against infections and is particularly effective against extracellular pathogens.
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8 Key excerpts on "Humoral Immunity"
eBook - ePubBasic Immunology E-Book
Basic Immunology E-Book
- Abul K. Abbas, Andrew H. Lichtman, Shiv Pillai(Authors)
- 2023(Publication Date)
- Elsevier(Publisher)
Humoral Immune Responses Activation of B Lymphocytes and Production of Antibodies- Phases and Types of Humoral Immune Responses
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Stimulation of B Lymphocytes by Antigen
- Antigen-Induced Signaling in B Cells
- Role of Innate Immune Signals in B Cell Activation
- Functional Consequences of B Cell Activation by Antigen
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Functions of Helper T Lymphocytes in Humoral Immune Responses
- Activation and Migration of Helper T Cells and B Cells
- Presentation of Antigens by B Lymphocytes to Helper T Cells
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Mechanisms of Helper T Cell–Mediated Activation of B Lymphocytes
- Extrafollicular and Germinal Center Reactions
- Heavy-Chain Class (Isotype) Switching
- Affinity Maturation
- Generation of Plasma Cells and Memory B Cells
- Antibody Responses to T-Independent Antigens
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Regulation of Humoral Immune Responses
- Antibody Feedback
- B Cell Signal Attenuation by Other Inhibitory Receptors
- Summary
Humoral Immunity is mediated by antibodies and is the arm of the adaptive immune response that functions to neutralize and eliminate extracellular microbes and microbial toxins. It is the principal type of immune response against extracellular microbial protein antigens, as well as against nonprotein antigens, such as microbial capsular polysaccharides and lipids that cannot be recognized by most types of T cells. Antibodies are produced by B lymphocytes and their progeny. Naive B lymphocytes recognize antigens but do not secrete antibodies, and antigen-induced activation of these cells stimulates their differentiation into antibody-secreting plasma cells and memory cells.
eBook - PDF- Ruth Mayforth(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
IDI Antibody Overview Introduction In this chapter, an overview of the humoral immune system and of antibody structure, function, and biosynthesis is presented. Its aim is to set the stage for a discussion of recent developments in antibody technology, which is the focus of the remainder of this book. The Humoral Immune System A number of features of antibodies are particularly remarkable, making them amenable to a number of scientific and medical applications. Anti-bodies bind antigens (their ligands, which generally can be thought of as foreign macromolecules) with a high degree of specificity and can discriminate between two very closely related antigens. Another striking characteristic of antibodies is their diversity. Human beings can produce at least 10 7 (and potentially even more than 10 11 ) antibodies with different specificities. (The genetic mechanisms responsible for generating this vast repertoire are quite extraordinary and are described later in this chapter.) Antibody diversity is so great that virtually any foreign macro-molecule can be recognized. The diversity of antibodies, combined with their specificity, makes them ideal biomolecular tools for scientific, diag-nostic, and therapeutic purposes. The human immune system can be divided into two major compo-nents: the humoral immune system and the cell-mediated immune sys-tem. Each human has about 2 x 10 12 lymphocytes (types of white blood cells). There are two kinds of lymphocytes, T cells and B cells, which are represented in approximately equal numbers. Both B cells and T cells express antigen-specific receptors on their cell surface, called the immunoglobulin receptor (IgR) and the T-cell receptor (TCR), respec-1 2 1 Antibody Overview tively. These receptors are clonally distributed—that is, all of the immuno-globulins that a given B-cell clone expresses are identical and have exactly the same specificity for antigen. When stimulated, B cells can also secrete their immunoglobulins.
eBook - PDF- Arthur M. Silverstein(Author)
- 2012(Publication Date)
- Academic Press(Publisher)
3 Cellular versus Humoral Immunity: Determinants and Consequences of an Epic Nineteenth-Century Battle I N A major address to the congress of the British Medical Association in 1896, Lord Lister suggested that if ever there had been a romantic chapter in the history of pathology, it was certainly that concerned with theories of immunity. Lister's reference was to two epic but interrelated battles that had occupied pathologists, bacteriologists, and immunologists over the course of several decades—battles that saw opposing schools engage in passionate debate and a degree of vilification almost unknown in present-day science. When Lister spoke in 1896, the first of these great disputes was nearing its resolution. This one involved the question of the basic nature of the inflammatory reaction—whether inflammation is an abnormal response harmful to the host or a normal and beneficial component of its defensive armamentarium. However, the second of these battles had not yet been resolved and was still being fought in every journal and at every congress relating to the subject. Its focus was on the question of whether innate and acquired immunity to infection could be best explained by cellular or by humoral mechanisms. In that exciting decade when remarkable discoveries crowded close on one another's heels, when new mechanisms, new organisms, new diseases appeared with almost every issue of the journals, the protagonists from one or the other camp grasped each new item eagerly to bolster their own theory or to cast doubt upon that of the opposition. The lines that divided the two camps were fairly sharply drawn. Conceptually, the cellularists argued that the chief defense of the body 38 Cellular versus Humoral Immunity 39 against infection resided in the phagocytic and digestive powers of the macrophage and the microphage (the polymorphonuclear leukocyte).
- Mary Keogan, Eleanor M. Wallace, Paula O'Leary(Authors)
- 2006(Publication Date)
- Routledge(Publisher)
B A S I C I M M U N O L O G Y B cells differentiate into plasma cells that make antibody, or secreted immunoglobulin. Antibodies bind extracellular pathogens or toxins, bringing about their destruction. This is termed Humoral Immunity. Cell-mediated immunity provides protection against intracellular pathogens. Antigen- specific cytotoxic T cells kill virally infected cells in an attempt to eliminate the virus. Another T cell subset (helper T cells) activates macrophages to kill microorganisms that reside within intracellular vesicles. Both mechanisms are included in the term cell-mediated immunity. The features of innate and adaptive immunity are summarised in Table 1.2.1. INNATE AND ADAPTIVE IMMUNITY SHARE SOME EFFECTOR MECHANISMS The effector functions of antibody depend on recruiting cells and molecules of the innate immune system. Antibodies target pathogens and their toxic products for disposal by phagocytes. ◆ Antibodies bind and neutralise bacterial toxins. ◆ Antibodies opsonise bacteria, facilitating their ingestion and destruction by macrophages or neutrophils. ◆ Antibodies activate complement, which can lyse bacteria or opsonise microbes. Macrophages become more effective at killing organisms after interaction with helper T cells. 12 Table 1.2.1 Features of innate and adaptive immunity CHARACTERISTICS CELLS MOLECULES Innate immunity Rapid response within hours Macrophages Cytokines No unique specificity Neutrophils Complement No memory NK cells Acute phase proteins Natural opsonins Adaptive immunity Slower reponse ~5–6days T and B lymphocytes Antibodies Highly specific Plasma cells Cytokines Memory Section 1.4 Innate Immune Responses I Section 1.5 Innate Immune Responses II – The Complement System Section 1.7 Inflammation Section 1.11 How Does the Immune System See Antigen? Section 1.15 Immunoglobulin Function Section 1.17 Helper T Cell Activation Section 1.18 Cytotoxic T Cells CROSS REFERENCES
eBook - PDF- Peter Walzer, Melanie T. Cushion, Peter Walzer, Melanie T. Cushion(Authors)
- 2004(Publication Date)
- CRC Press(Publisher)
12 The Role of Humoral Immunity in the Defense Against Pneumocystis FRANCIS GIGLIOTTI, CONSTANTINE G. HAIDARIS, and TERRY W. WRIGHT University of Rochester Medical Center Rochester, New York, U.S.A. ALLEN G. HARMSEN Montana State University Bozeman, Montana, U.S.A. I. Introduction The immune system comprises a complex organization of innate and adaptive host defenses involving multiple organs. These include organ systems with mucosal surfaces, such as the respiratory and alimentary tracts, that encounter the bulk of the microbes to which we are exposed. The circulatory and lymphatic systems are classically thought of as contributing cellular and humoral adaptive immune mechanisms against infection. Nontraditional ‘‘immune’’ organ systems such as the central nervous and endocrine systems also participate in immunity against infection. As our understanding of immune defense mechanisms deepens, we come to see that the defense against most microorganisms is usually multifacto-rial. Thus, while it may be somewhat artificial to focus on a single aspect of the immune response in the defense against an infectious agent, such an approach may be useful in helping us to understand how various elements of host immunity can bring about control of an infection. In this chapter, we summarize the evidence that antibody-mediated immunity is critical in protecting against the development of Pneumocystis pneumonia (PcP), knowing full well that many components of the immune system interact to control disease produced by Pneumocystis . We also briefly describe examples of antibody-mediated immunity against other fungi as models that may provide a guide for future studies on Pneumocystis . 269 Gigliotti et al. 270 II. Observations in Humans A. Seroprevalence and Age-Dependent Seroconversion to Pneumocystis Serological screens of normal populations can often be an important tool to deter-mine the prevalence of an infection in the population.
eBook - ePub- Arthur M. Silverstein(Author)
- 2009(Publication Date)
- Academic Press(Publisher)
Chapter 2. Cellular vs Humoral Immunity....one of Metchnikoff's most suggestive biological romances...George Bernard Shaw, The Doctor's DilemmaIn a major address to the congress of the British Medical Association in 1896, Lord Lister suggested that if ever there had been a romantic chapter in the history of pathology, it was certainly that concerned with theories of immunity. Lister's reference was to two epic but interrelated battles that had occupied pathologists, bacteriologists, and immunologists over the course of several decades – battles which saw opposing schools engage in passionate debate and a degree of vilification almost unknown in present-day science. When Lister spoke in 1896, the first of these great disputes was nearing its resolution. This involved the question of the basic nature of the inflammatory reaction – whether inflammation is an abnormal response harmful to the host, or a normal and beneficial component of its defensive armamentarium. However, the second of these battles had not yet been resolved, and was still being fought in every journal and at every congress relating to the subject. Its focus was on the question of whether innate and acquired immunity to infection could be best explained by cellular or by humoral mechanisms. In that exciting decade when remarkable discoveries crowded close on one another's heels, when new mechanisms, new organisms, new diseases appeared with almost every issue of the journals, the protagonists from one or the other camp grasped each new item eagerly to bolster their own theory, or to cast doubt upon that of the opposition.The lines that divided the two camps were fairly sharply drawn. Conceptually, the cellularists argued that the chief defense of the body against infection resided in the phagocytic and digestive powers of the macrophage and the microphage (the polymorphonuclear leukocyte), while the humoralists claimed that only the soluble substances of the blood and other body fluids could immobilize and destroy invading pathogens. Geographically, the cellularists were predominantly French and rallied round Elie Metchnikoff at the Pasteur Institute in Paris, while the humoralists were predominantly German and followed the leadership of Robert Koch and his disciples at Koch's Institute in Berlin.
eBook - PDFMicrobiology
Principles and Explorations
- Jacquelyn G. Black, Laura J. Black(Authors)
- 2018(Publication Date)
- Wiley(Publisher)
Humoral Immunity 483 complement system; IgA is less powerful. Sometimes, an- tibodies, especially IgM, directly lyse cell membranes of infectious agents without the aid of complement. Bacterial toxins, being small molecules secreted from the cell, usually are inactivated simply by the formation of antigen-antibody complexes, or neutralization. IgG is the main neutralizer of bacterial toxins. Neutralization effectively stops the toxin from doing further damage to the host. It does not destroy the organisms that produce the toxin—antibiotics are needed to prevent persisting organisms from continuing to produce toxin. Viruses, too, can be inactivated by neutralization (Figure 18.11a); IgM, IgG, and IgA are all effective neutralizers of viruses. Those viruses that have an envelope may then be lysed by complement (Figure 18.11b). We have now considered the major characteristics of Humoral Immunity—how B cells are activated, how anti- bodies are produced, and how they function. These pro- cesses are summarized in Figure 18.12. the body and can be made to occur in the laboratory. Here we will describe reactions chiefly as they relate to destruction of pathogens. We will discuss their labora- tory applications more fully in ▶ Chapter 19. Because bacterial cells are relatively large particles, the particles that result from antigen-antibody reac- tions also are large. Such reactions result in agglutination (ag-lu-tin-a′shun), or the sticking together of microbes. IgM produces strong, and IgG produces weak, agglutina- tion reactions with certain bacterial cells. Agglutination reactions produce results that are visible to the unaided eye and can be used as the basis of laboratory tests to detect the presence of antibodies or antigens. Some an- tibodies act as opsonins ( ◀ Chapter 17). That is, they neutralize toxins and coat microbes so that they can be phagocytized, a process called opsonization.
eBook - PDF- Cecie Starr, Beverly McMillan(Authors)
- 2015(Publication Date)
- Cengage Learning EMEA(Publisher)
Due to electronic rights, some third party content may be suppressed from the eBook and/or eChapter(s). Editorial review has deemed that any suppressed content does not materially affect the overall learning experience. Cengage Learning reserves the right to remove additional content at any time if subsequent rights restrictions require it. 164 CHAPTER 9 This antibody can bind to a type of virus This antibody can bind to a species of bacteria immunoglobulin Ig; an antibody. Antibodies: Defense against Threats outside Cells Because of the great diversity of antigen receptors, there’s a good chance the lymph node also contains an inactive B cell with receptors for the invader’s antigen. If so, the B cell binds to the bacterial antigen and displays it (again, in an antigen–MHC complex) at the B cell’s surface (Figure 9.12B). This processing activates the B cell. It also allows helper T cells in the node to recognize and bind to the antigen–MHC complex. Now the T cell and active B cell can interact. The T cell begins to release cytokines that spur the B cell to divide. Its descendants become plasma cells or memory B cells. The plasma cells release huge numbers of antibodies into the bloodstream—up to 2,000 each minute. When any of these antibodies binds to an antigen, it marks the invader for destruction by phagocytes and complement proteins. The memory B cells will be available to respond quickly to the antigen if it attacks the body another time. n Antibodies flag invaders or toxins so that the pathogens can be destroyed or eliminated. Antibody-mediated immune responses produce a flood of antibodies Antibodies don’t kill pathogens or directly destroy toxins in body fluids. Instead, antibodies mark these invaders so that other mechanisms prevent them from harming body cells. When a B cell forms, the genetic mechanisms involved ensure that it has receptors for only one antigen—such as a particular bacterial or viral protein.
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