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In immunology, an antigen (Ag) is a molecule, moiety, foreign particulate matter, or an allergen, such as pollen, that can bind to a specific antibody or T-cell receptor. The presence of antigens in the body may trigger an immune response.
The T helper cells (Th cells), also known as CD4+ cells or CD4-positive cells, are a type of T cell that play an important role in the adaptive immune system. They aid the activity of other immune cells by releasing cytokines. They are considered essential in B cell antibody class switching, breaking cross-tolerance in dendritic cells, in the activation and growth of cytotoxic T cells, and in maximizing bactericidal activity of phagocytes such as macrophages and neutrophils. CD4+ cells are mature Th cells that express the surface protein CD4. Genetic variation in regulatory elements expressed by CD4+ cells determines susceptibility to a broad class of autoimmune diseases.
Natural killer cells, also known as NK cells or large granular lymphocytes (LGL), are a type of cytotoxic lymphocyte critical to the innate immune system that belong to the rapidly expanding family of known innate lymphoid cells (ILC) and represent 5–20% of all circulating lymphocytes in humans. The role of NK cells is analogous to that of cytotoxic T cells in the vertebrate adaptive immune response. NK cells provide rapid responses to virus-infected cell and other intracellular pathogens acting at around 3 days after infection, and respond to tumor formation. Typically, immune cells detect the antigen presented on major histocompatibility complex (MHC) on infected cell surfaces, triggering cytokine release, causing the death of the infected cell by lysis or apoptosis. NK cells are unique, however, as they have the ability to recognize and kill stressed cells in the absence of antibodies and MHC, allowing for a much faster immune reaction. They were named "natural killers" because of the notion that they do not require activation to kill cells that are missing "self" markers of MHC class 1. This role is especially important because harmful cells that are missing MHC I markers cannot be detected and destroyed by other immune cells, such as T lymphocyte cells.
In immunology, anergy is a lack of reaction by the body's defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance. An individual in a state of anergy often indicates that the immune system is unable to mount a normal immune response against a specific antigen, usually a self-antigen. Lymphocytes are said to be anergic when they fail to respond to their specific antigen. Anergy is one of three processes that induce tolerance, modifying the immune system to prevent self-destruction.
Superantigens (SAgs) are a class of antigens that result in excessive activation of the immune system. Specifically they cause non-specific activation of T-cells resulting in polyclonal T cell activation and massive cytokine release. SAgs are produced by some pathogenic viruses and bacteria most likely as a defense mechanism against the immune system. Compared to a normal antigen-induced T-cell response where 0.0001-0.001% of the body's T-cells are activated, these SAgs are capable of activating up to 20% of the body's T-cells. Furthermore, Anti-CD3 and Anti-CD28 antibodies (CD28-SuperMAB) have also shown to be highly potent superantigens.
The T-cell receptor (TCR) is a protein complex found on the surface of T cells, or T lymphocytes, that is responsible for recognizing fragments of antigen as peptides bound to major histocompatibility complex (MHC) molecules. The binding between TCR and antigen peptides is of relatively low affinity and is degenerate: that is, many TCRs recognize the same antigen peptide and many antigen peptides are recognized by the same TCR.
An immune complex, sometimes called an antigen-antibody complex or antigen-bound antibody, is a molecule formed from the binding of multiple antigens to antibodies. The bound antigen and antibody act as a unitary object, effectively an antigen of its own with a specific epitope. After an antigen-antibody reaction, the immune complexes can be subject to any of a number of responses, including complement deposition, opsonization, phagocytosis, or processing by proteases. Red blood cells carrying CR1-receptors on their surface may bind C3b-coated immune complexes and transport them to phagocytes, mostly in liver and spleen, and return to the general circulation.
Cluster of Differentiation 86 is a protein constitutively expressed on dendritic cells, Langerhans cells, macrophages, B-cells, and on other antigen-presenting cells. Along with CD80, CD86 provides costimulatory signals necessary for T cell activation and survival. Depending on the ligand bound, CD86 can signal for self-regulation and cell-cell association, or for attenuation of regulation and cell-cell disassociation.
Emil Raphael Unanue was a Cuban-American immunologist and Paul & Ellen Lacy Professor Emeritus at Washington University School of Medicine. He is a member of the National Academy of Sciences, the American Academy of Arts and Sciences and the Institute of Medicine. He previously served as chair of the National Academy of Sciences Section of Microbiology and Immunology.
Polyclonal B cell response is a natural mode of immune response exhibited by the adaptive immune system of mammals. It ensures that a single antigen is recognized and attacked through its overlapping parts, called epitopes, by multiple clones of B cell.
Harald von Boehmer was a German-Swiss immunologist best known for his work on T cells.
The following outline is provided as an overview of and topical guide to immunology:
In immunology, clonal deletion is the removal through apoptosis of B cells and T cells that have expressed receptors for self before developing into fully immunocompetent lymphocytes. This prevents recognition and destruction of self host cells, making it a type of negative selection or central tolerance. Central tolerance prevents B and T lymphocytes from reacting to self. Thus, clonal deletion can help protect individuals against autoimmunity. Clonal deletion is thought to be the most common type of negative selection. It is one method of immune tolerance.
James Patrick Allison is an American immunologist and Nobel laureate who holds the position of professor and chair of immunology and executive director of immunotherapy platform at the MD Anderson Cancer Center at the University of Texas.
Mark Morris Davis is an American immunologist. He is the director of and Avery Family Professor of Immunology at the Institute for Immunity, Transplantation and Infection at Stanford University.
Jean Sylvia Marshall, born in Birmingham, England, is a Canadian immunologist and acting Professor and Head of the Department of Microbiology & Immunology at Dalhousie University in Halifax, Nova Scotia, Canada. Marshall's work has investigated how mast cells are involved in the early immune response to infection and antigen. She is best known for her discovery of the previously unknown degranulation-independent immunoregulatory roles of mast cells in infection and allergy and their ability to mobilize dendritic cells.
Garnett Herrel Kelsoe is an American immunologist and the James B. Duke Professor of Immunology at Duke University School of Medicine.
Sebastian Amigorena is an Argentinian-French immunologist and a Team Leader at the Institut Curie.
Tania H. Watts is a Canadian Immunologist, Professor at the University of Toronto, past President of the Canadian Society for Immunology and from 2009-2019 held the Sanofi Pasteur Chair in Human Immunology at the University of Toronto. Tania Watts holds a Tier 1 Canada Research Chair in Anti-viral Immunity and was named a Distinguished Fellow of the American Association of Immunologists, class of 2022.
Marc K. Jenkins is a Regents Professor and Director of the Center for Immunology at the University of Minnesota. He is a member of the National Academy of Sciences.
References
- 1 2 3 Allen, Paul M. (2006). "Defining Yourself: Tolerance Development in the Immune System". The Journal of Immunology. 177 (3): 1369–1372. doi: 10.4049/jimmunol.177.3.1369 . PMID 16849437.
- ↑ "Paul Allen, PhD". Washington University School of Medicine. Retrieved 15 July 2019.
- ↑ ProQuest Dissertations and Theses - Paul Malone Allen (Ph.D). 1981. ProQuest 303128284 . Retrieved 15 July 2019– via ProQuest.
- ↑ "Paul M. Allen, PhD". AAI. Retrieved 15 July 2019.
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