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16-September-2008 16:15:15 - immune system See also: Immune system, Passive immunity, and Innate immune system A scanning electron microscope SEM image of a single human lymphocyte. A scanning electron microscope SEM image of a single human lymphocyte. The adaptive immune system is composed of highly specialized, systemic cells and processes that eliminate or prevent pathogenic challenges. Thought to have arisen in the first jawed vertebrates, the adaptive or specific immune system is activated by the non-specific and evolutionarily older innate immune system which is the major system of host defense against pathogens in nearly all other living things. The adaptive immune response provides the vertebrate immune system with the ability to recognize and remember specific pathogens to generate immunity, and to mount stronger attacks each time the pathogen is encountered. It is adaptive immunity because the body's immune system prepares itself for future challenges. The system is highly adaptable because of somatic hypermutation a process of accelerated somatic mutations, and VDJ recombination an irreversible genetic recombination of antigen receptor gene segments. This mechanism allows a small number of genes to generate a vast number of different antigen receptors, which are then uniquely expressed on each individual lymphocyte. Because the gene rearrangement leads to an irreversible change in the DNA of each cell, all of the progeny of that cell will then inherit genes encoding the same receptor specificity, including the Memory B cells and Memory T cells that are the keys to long-lived specific immunity. Contents 1 Functions 2 Effector cells 3 Antigen presentation 3.1 Exogenous antigens 3.2 Endogenous antigens 4 T lymphocytes 4.1 CD8+ T lymphocytes and cytotoxicity 4.2 Helper T-cells 4.2.1 Th1 and Th2: helper T cell responses 4.3 γδ T cells 5 B lymphocytes and antibody production 6 Alternative adaptive immune system 7 Immunological memory 7.1 Passive memory 7.2 Active Memory 7.2.1 Immunization 8 Immunological diversity 9 Adaptive immunity during pregnancy 10 See also 11 References Functions Adaptive immunity is triggered in vertebrates when a pathogen evades the innate immune system and generates a threshold level of antigen.1 The major functions of the adaptive immune system include: The recognition of specific non-self antigens in the presence of self, during the process of antigen presentation. The generation of responses that are tailored to maximally eliminate specific pathogens or pathogen infected cells. The development of immunological memory, in which each pathogen is remembered by a signature antigen. These memory cells can be called upon to quickly eliminate a pathogen should subsequent infections occur. Effector cells Main article: Lymphocyte The cells of the adaptive immune system are a type of leukocyte, called a lymphocyte. B cells and T cells are the major types of lymphocytes. The human body has about 2 trillion lymphocytes, constituting 20-40% of white blood cells WBCs; their total mass is about the same as the brain or liver.2 The peripheral blood contains 20-50% of circulating lymphocytes; the rest move within the lymphatic system.2 B cells and T cells are derived from the same pluripotential hematopoietic stem cells, and are indistinguishable from one another until after they are activated.3 B cells play a large role in the humoral immune response, whereas T-cells are intimately involved in cell-mediated immune responses. B-cells may be named for the bursa of Fabricius, an organ unique to birds, where the cells were first found to develop. However, in nearly all other vertebrates, B cells and T-cells are produced by stem cells in the bone marrow.3 T-cells travel to and develop in the thymus, from which they derive their name. In humans, approximately 1-2% of the lymphocyte pool recirculates each hour to optimize the opportunities for antigen-specific lymphocytes to find their specific antigen within the secondary lymphoid tissues.4 In an adult animal, the peripheral lymphoid organs contain a mixture of B- and T cells in at least three stages of differentiation: naive cells that have matured, left the bone marrow or thymus, have entered the lymphatic system, but that have yet to encounter their cognate antigen, effector cells that have been activated by their cognate antigen, and are actively involved in eliminating a pathogen and, memory cells - the long-lived survivors of past infections. Antigen presentation Main article: Antigen presentation Adaptive immunity relies on the capacity of immune cells to distinguish between the body's own cells and unwanted invaders. Association between TCR and MHC class I or MHC class II Association between TCR and MHC class I or MHC class II The host's cells express self antigens. These antigens are different from those on the surface of bacteria non-self antigens or on the surface of virally infected host cells missing-self. The adaptive response is triggered by recognizing non-self and missing-self antigens. With the exception of non-nucleated cells including erythrocytes, all cells are capable of presenting antigen and of activating the adaptive response.3 Some cells are specially equipped to present antigen, and to prime naive T cells. Dendritic cells and B-cells and to a lesser extent macrophages are equipped with special immunostimulatory receptors that allow for enhanced activation of T cells, and are termed professional antigen presenting cells APC. Several T cells subgroups can be activated by professional APCs, and each type of T cell is specially equipped to deal with each unique toxin or bacterial and viral pathogen. The type of T cell activated, and the type of response generated, depends in part, on the context in which the APC first encountered the antigen.1 Exogenous antigens Antigen presentation stimulates T cells to become either cytotoxic CD8+ cells or helper CD4+ cells Antigen presentation stimulates T cells to become either cytotoxic CD8+ cells or helper CD4+ cells 5 Dendritic cells engulf exogenous pathogens, such as bacteria, parasites or toxins in the tissues and then migrate, via chemotactic signals, to the T cell enriched lymph nodes. During migration, dendritic cells undergo a process of maturation in which they lose most of their ability to engulf other pathogens and develop an ability to communicate with T-cells. The dendritic cell uses enzymes to chop the pathogen into smaller pieces, called antigens. In the lymph node, the dendritic cell will display these non-self antigens on its surface by coupling them to a self-receptor called the Major histocompatibility complex, or MHC also known in humans as Human leukocyte antigen HLA.1 This MHC:antigen complex is recognized by T-cells passing through the lymph node. Exogenous antigens are usually displayed on MHC class II molecules, which activate CD4+ helper T-cells.1 Endogenous antigens Endogenous antigens are produced by viruses replicating within a host cell.1 The host cells use enzymes to digest virally associated proteins, and displays these pieces on its surface to T-cells by coupling them to MHC. Endogenous antigens are typically displayed on MHC class I molecules, and activate CD8+ cytotoxic T-cells. With the exception of non-nucleated cells including erythrocytes, MHC class I is expressed by all host cells.1 T lymphocytes Main article: T cell CD8+ T lymphocytes and cytotoxicity Main article: Cytotoxic T cell Cytotoxic T cells also known as TC, killer T cell, or cytotoxic T-lymphocyte CTL are a sub-group of T cells which induce the death of cells that are infected with viruses and other pathogens, or are otherwise damaged or dysfunctional.1 Killer T cells-also called cytotoxic T lymphocytes or CTL-directly attack other cells carrying certain foreign or abnormal molecules on their surfaces. Killer T cells-also called cytotoxic T lymphocytes or CTL-directly attack other cells carrying certain foreign or abnormal molecules on their surfaces5. Naive cytotoxic T cells are activated when their T-cell receptor TCR strongly interacts with a peptide-bound MHC class I molecule. This affinity depends on the type and orientation of the antigen/MHC complex, and is what keeps the CTL and infected cell bound together.1 Once activated, the CTL undergoes a process called clonal expansion in which it gains functionality, and divides rapidly, to produce an army of armed-effector cells. Activated CTL will then travel throughout the body in search of cells bearing that unique MHC Class I + peptide. When exposed to these infected or dysfunctional somatic cells, effector CTL release perforin and granulysin: cytotoxins which form pores in the target cell's plasma membrane, allowing ions and water to flow into the infected cell, and causing it to burst or lyse.1 CTL release granzyme, a serine protease that enters cells via pores to induce apoptosis cell death. To limit extensive tissue damage during an infection, CTL activation is tightly controlled and generally requires a very strong MHC/antigen activation signal, or additional activation signals provided by helper T-cells see below.1 Upon resolution of the infection, most of the effector cells will die and be cleared away by phagocytes, but a few of these cells will be retained as memory cells.3 Upon a later encounter with the same antigen, these memory cells quickly differentiate into effector cells, dramatically shortening the time required to mount an effective response. Helper T-cells Main article: T helper cell The T lymphocyte activation pathway. T cells contribute to immune defenses in two major ways: some direct and regulate immune responses; others directly attack infected or cancerous cells. The T lymphocyte activation pathway. T cells contribute to immune defenses in two major ways: some direct and regulate immune responses; others directly attack infected or cancerous cells5. CD4+ lymphocytes, or helper T cells, are immune response mediators, and play an important role in establishing and maximizing the capabilities of the adaptive immune response.1 These cells have no cytotoxic or phagocytic activity; and cannot kill infected cells or clear pathogens, but, in essence manage the immune response, by directing other cells to perform these tasks. Helper T cells express T-cell receptors TCR that recognize antigen bound to Class II MHC molecules. The activation of a naive helper T-cell causes it to release cytokines, which influences the activity of many cell types, including the APC that activated it. Helper T-cells require a much milder activation stimulus than cytotoxic T-cells. Helper T-cells can provide extra signals that help activate cytotoxic cells.3 Th1 and Th2: helper T cell responses Two types of effector CD4+ T helper cell responses can be induced by a professional APC, designated Th1 and Th2, each designed to eliminate different types of pathogens. The factors that dictate whether an infection will trigger a Th1 or Th2 type response are not fully understood, but the response generated does play an important role in the clearance of different pathogens.1 The Th1 response is characterized by the production of Interferon-gamma, which activates the bactericidal activities of macrophages, and induces B-cells to make opsonizing coating antibodies, and leads to cell-mediated immunity 1. The Th2 response is characterized by the release of Interleukin 4, which results in the activation of B-cells to make neutralizing killing antibodies, leading to humoral immunity.1 Generally, Th1 responses are more effective against intracellular pathogens viruses and bacteria that are inside host cells, while Th2 responses are more effective against extracellular bacteria, parasites and toxins1. Like cytotoxic T-cells, most of the CD4+ helper cells will die upon resolution of infection, with a few remaining as CD4+ memory cells. HIV is able to subvert the immune system by attacking the CD4+ T cells, precisely the cells that could drive the destruction of the virus, but also the cells that drive immunity against all other pathogens encountered during an organisms' lifetime.3 A third type of T lymphocyte, the regulatory T cells Treg, limits and suppresses the immune system, and may control aberrant immune responses to self-antigens; an important mechanism in controlling the development of autoimmune diseases.3 γδ T cells Main article: gamma/delta T cells γδ T cells possess an alternative T cell receptor TCR as opposed to CD4+ and CD8+ αβ T cells and share characteristics of helper T cells, cytotoxic T cells and natural killer cells. Like other 'unconventional' T cell subsets bearing invariant TCRs, such as CD1d-restricted Natural Killer T cells, γδ T cells exhibit characteristics that place them at the border between innate and adaptive immunity. On one hand, γδ T cells may be considered a component of adaptive immunity in that they rearrange TCR genes to produce junctional diversity and develop a memory phenotype. On the other hand however, the various subsets may also be considered part of the innate immune system where a restricted TCR and/or NK receptors may be used as a pattern recognition receptor. For example, according to this paradigm, large numbers of Vγ9/Vδ2 T cells respond within hours to common molecules produced by microbes, and highly restricted intraepithelial Vδ1 T cells will respond to stressed epithelial cells. B lymphocytes and antibody production Main article: B cell The B lymphocyte activation pathway. B cells function to protect the host by producing antibodies that identify and neutralize foreign objects like bacteria and viruses. The B lymphocyte activation pathway. B cells function to protect the host by producing antibodies that identify and neutralize foreign objects like bacteria and viruses.5 B Cells are the major cells involved in the creation of antibodies that circulate in blood plasma and lymph, known as humoral immunity. Antibodies or immunoglobulin, Ig, are large Y-shaped proteins used by the immune system to identify and neutralize foreign objects. In mammals there are five types of antibody: IgA, IgD, IgE, IgG, and IgM, differing in biological properties, each has evolved to handle different kinds of antigens. Upon activation, B cells produce antibodies, each of which recognizes a unique antigen, and neutralize specific pathogens.1 Like the T cell receptor, B cells express a unique B cell receptor BCR, in this case, an immobilized antibody molecule. The BCR recognizes and binds to only one particular antigen. A critical difference between B cells and T cells is how each cell sees an antigen. T cells recognize their cognate antigen in a processed form - as a peptide in the context of an MHC molecule,1 while B cells recognize antigens in their native form.1 Once a B cell encounters its cognate or specific antigen and receives additional signals from a helper T cell predominately Th2 type, it further differentiates into an effector cell, known as a plasma cell.1 Plasma cells are short lived cells 2-3 days which secrete antibodies. These antibodies bind to antigens, making them easier targets for phagocytes, and trigger the complement cascade.1 About 10% of plasma cells will survive to become long-lived antigen specific memory B cells.1 Already primed to produce specific antibodies, these cells can be called upon to respond quickly if the same pathogen re-infects the host; while the host experiences few, if any, symptoms. Alternative adaptive immune system Although the classical molecules of the adaptive immune system e.g. antibodies and T cell receptors exist only in jawed vertebrates, a distinct lymphocyte-derived molecule has been discovered in primitive jawless vertebrates, such as the lamprey and hagfish. These animals possess a large array of molecules called variable lymphocyte receptors VLRs for short that, like the antigen receptors of jawed vertebrates, are produced from only a small number one or two of genes. These molecules are believed to bind pathogenic antigens in a similar way to antibodies, and with the same degree of specificity.6 Immunological memory For more details on this topic, see Immunity medical. When B cells and T cells are activated some will become memory cells. Throughout the lifetime of an animal these memory cells form a database of effective B and T lymphocytes, for which upon interaction with a previously encountered antigen the appropriate memory cells are selected and activated, in this manner a stronger immune response can be produced quicker on the second and proceeding exposures to an antigen. This is adaptive because the body's immune system prepares itself for future challenges. Immunological memory can either be in the form of passive short-term memory or active long-term memory. Passive memory Passive memory is usually short-term, lasting between a few days and several months. Newborn infants have had no prior exposure to microbes and are particularly vulnerable to infection. Several layers of passive protection are provided by the mother. In utero, maternal IgG is transported directly across the placenta, so that at birth, human babies have high levels of antibodies, with the same range of antigen specificities as their mother.1 Breast milk contains antibodies that are transferred to the gut of the infant, protecting against bacterial infections, until the newborn can synthesize its own antibodies.1 This is passive immunity because the fetus does not actually make any memory cells or antibodies, it only borrows them. Short-term passive immunity can also be transferred artificially from one individual to another via antibody-rich serum. Active Memory Active immunity is generally long-term and can be acquired by infection followed by B cells and T cells activation, or artificially acquired by vaccines, in a process called immunization. Immunization Historically, infectious disease has been the leading cause of death in the human population. Over the last century, two important factors have been developed to combat their spread; sanitation and immunization.3 Immunization commonly referred to as vaccination is the deliberate induction of an immune response, and represents the single most effective manipulation of the immune system mankind has developed.3 Immunizations are successful because they utilize the immune system's natural specificity as well as its inducibility. The principle behind immunization is to introduce an antigen, derived from a disease causing organism, that stimulates the immune system to develop protective immunity against that organism, but which does not itself cause the pathogenic effects of that organism. An antigen short for antibody generator, is defined as any substance that binds to a specific antibody and elicits an adaptive immune response.2 Most viral vaccines are based on live attenuated viruses, while many bacterial vaccines are based on acellular components of micro-organisms, including harmless toxin components.2 Many antigens derived from acellular vaccines do not strongly induce an adaptive response, and most bacterial vaccines require the addition of adjuvants that activate the antigen presenting cells of the innate immune system to enhance immunogenicity.3 Immunological diversity Most large molecules, including virtually all proteins and many polysaccharides, can serve as antigens.1 The parts of an antigen that interact with an antibody molecule or a lymphocyte receptor, are called epitopes. Most antigens contain a variety of epitopes and can stimulate the production of antibodies, specific T cell responses, or both.1 An antibody is made up of two heavy chains and two light chains. The unique variable region allows an antibody to recognize its matching antigen. An antibody is made up of two heavy chains and two light chains. The unique variable region allows an antibody to recognize its matching antigen.5 A very small proportion less than 0.01% of the total lymphocytes are able to bind to a particular antigen, which suggests that only a few cells will respond to each antigen.3 For the adaptive response to remember and eliminate a large number of pathogens the immune system must be able to distinguish between many different antigens,2 and the receptors that recognize antigens must be produced in a huge variety of configurations, essentially one receptor for each different pathogen that might ever be encountered. Even in the absence of antigen stimulation, a human is capable of producing more than 1 trillion different antibody molecules.3 Millions of genes would be required to store the genetic information used to produce these receptors, but, the entire human genome contains fewer than 25,000 genes.7 This myriad of receptors are produced through a process known as clonal selection.12 According to the clonal selection theory, at birth, an animal will randomly generate a vast diversity of lymphocytes each bearing a unique antigen receptor from information encoded in a small family of genes. In order to generate each unique antigen receptor, these genes will have undergone a process called combinatorial diversification, in which one gene segment recombines with other gene segments to form a single unique gene. It is this assembly process that generates the enormous diversity of receptors and antibodies, before the body ever encounters antigens, and enables the immune system to respond to an almost unlimited diversity of antigens.1 Throughout the lifetime of an animal, those lymphocytes that can react against the antigens an animal actually encounters, will be selected for action, directed against anything that expresses that antigen. It is important to note that the innate and adaptive portions of the immune system work together and not in spite of each other. The adaptive arm, B and T cells, would be unable to function without the input of the innate system. T cells are useless without antigen-presenting cells to activate them, and B cells are crippled without T-cell help. On the other hand, the innate system would likely be overrun with pathogens without the specialized action of the adaptive immune response. Adaptive immunity during pregnancy The cornerstone of the immune system is the recognition of self versus non-self. Therefore, the mechanisms which protect the human fetus which is considered non-self from attack by the immune system, are particularly interesting. Although no comprehensive explanation has emerged to explain this mysterious, and often repeated, lack of rejection, two classical reasons may explain how the fetus is tolerated. The first is that the fetus occupies a portion of the body protected by a non-immunological barrier, the uterus, which the immune system does not routinely patrol.1 The second is that the fetus itself may promote local immunosuppression in the mother, perhaps by a process of active nutrient depletion.1 A more modern explanation for this induction of tolerance is that specific glycoproteins expressed in the uterus during pregnancy suppress the uterine immune response see eu-FEDS. See also Wikimedia Commons has media related to: Immunology Affinity maturation Allelic exclusion Anergy Immune tolerance Immunosuppression Original antigenic sin Somatic hypermutation VDJ recombination Polyclonal response References ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac Janeway, Charles; Paul Travers, Mark Walport, and Mark Shlomchik 2001. Immunobiology; Fifth ion. New York and London: Garland Science. ISBN 0-8153-4101-6. . ^ a b c d e f Alberts, Bruce; Alexander Johnson, Julian Lewis, Martin Raff, Keith Roberts, and Peter Walters 2002. Molecular Biology of the Cell; Fourth ion. New York and London: Garland Science. ISBN 0-8153-3218-1. ^ a b c d e f g h i j k l Janeway CA, Jr. et al 2005. Immunobiology., 6th ed., Garland Science. ISBN 0-443-07310-4. ^ Microbiology and Immunology On-Line Textbook: USC School of Medicine ^ a b c d e The NIAID resource booklet Understanding the Immune System pdf. ^ M.N. Alder, I.B. Rogozin, L.M. Iyer, G.V. Glazko, M.D. Cooper, Z. Pancer 2005. Diversity and Function of Adaptive Immune Receptors in a Jawless Vertebrate. Science 310 5756: 1970-1973. doi:10.1126/science.1119420. PMID 16373579. ^ International Human Genome Sequencing Consortium 2004. Finishing the euchromatic sequence of the human genome. Nature 431 7011: 931-45. doi:10.1038/nature03001. PMID 15496913. v d e Immune system / Immunology Systems Adaptive immune system vs. Innate immune system · Humoral immune system vs. Cellular immune system · Complement system Anaphylatoxins · Intrinsic immune system Antibodies and antigens Antibody Monoclonal antibodies, Polyclonal antibodies, Autoantibody · Allotype · Isotype · Idiotype · Antigen Superantigen · Polyclonal B cell response Immune cells/White blood cells Lymphoid: T cell · B cell · NK cell Myeloid: Mast cell · Basophil · Eosinophil · Macrophage Phagocytes: Neutrophil · Macrophage/Reticuloendothelial system Professional APCs: Dendritic cell · Macrophage · B cell Immunity vs. tolerance Immunity · Autoimmunity · Allergy · Tolerance Central · Immunodeficiency Immunogenetics Somatic hypermutation · VDJ recombination · Immunoglobulin class switching · MHC/HLA Substances Cytokines · Opsonin · Cytolysin Other Inflammation · Epitope Linear epitope and Conformational epitope · Hapten · Cross-reactivity · Diagnostic immunology · Immune complex v d e Immune system: Lymphatic system Lymph, Lymphocytes Primary Bone marrow - Thymus Hassall's corpuscles Secondary: Spleen process blood Hilum - Trabeculae Red pulp Cords of Billroth, Marginal zone White pulp Periarteriolar lymphoid sheaths, Germinal center Trabecular arteries - Trabecular veins Secondary: Lymph nodes process extracellular fluid Afferent lymph vessels - Cortical sinuses - Medullary sinuses - Efferent lymph vessels T cells: High endothelial venules B cells: Primary follicle/Germinal center - Mantle zone - Marginal zone Lymph node capsule - Subcapsular sinus - Cortex - Paracortex - Medulla Medullary cord - Hilus Lymph node trabeculae Secondary: MALT process mucosa GALT - Peyer's patches - Germinal center v d e Human organ systems Cardiovascular system Digestive system Endocrine system Immune system Integumentary system Lymphatic system Muscular system Nervous system Reproductive system Respiratory system Skeletal system Urinary system Retrieved from http://en..org/wiki/Adaptive_immune_system Categories: Immune system Views Article Discussion this page History Personal tools Log in / create account Navigation Main page Contents Featured content Current events Random article Search Go Search Interaction Community portal Recent changes Contact Donate to Help Toolbox What links here Related changes Upload file Special pages Printable version Permanent link Cite this page Languages Italiano Português РуÑ?Ñ?кий Türkçe Suomi This page was last modified on 23 July 2008, at 08:29
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