Schematic diagram of B lymphocyte activation leading to plasma cell and B memory cell formation. B cells are activated by the binding of antigen to antibodies expressed on their surface. As an antigen-presenting cell, a B cell internalizes the antibody-antigen complex, partially digests the antigen, and then displays parts of it on the surface of its own MHC II molecules. The T cell receptor (TCRj on a
proteins are displayed in the context of MHC I molecules to interact with cytotoxic CD81 T lymphocytes, b. On antigen-presenting cells (e.g., macrophages), the foreign antigen is displayed in the context of MHC II molecules to interact with a helper CD4+ T lymphocyte.
memory B cells helper CD4+ T lymphocyte recognizes both the antigen and the MHC II molecule, activating the helper CD4+ T lymphocyte. The activated helper CD4+ T lymphocyte releases interleukins IL-2, IL-4, IL-5, and IL-6, which promote division and differentiation of the B lymphocyte into plasma cells and memory B cells. Ab, antibody; Ag, antigen.
memory B cells complex. These complexes are eliminated in a variety of ways, including destruction by NK cells and phagocytosis by macrophages and eosinophils. NI< cells recognize the Fc region of antibodies and preferentially attack and destroy target cells, usually those coated with IgG antibodies (Fig. 13.7). NI< cells act in concert with killer (K) cells and antibody-dependent cell-mediated cytotoxicity (ADCC) cells to induce the lysis of target cells, most commonly through the action of tumor-specific antibodies. ADCC reactions involve binding of an antibody or antibody and complement-coated target cell to an effector cell (NK, K, ADCC) bearing a receptor for the Fc portion of the antibody (see Fig. 13.2). This binding (through the Fc region) results in the lysis of the target cell.
If the antigen is a bacterium, the antigen-antibody complex may also activate a system of plasma proteins called the complement system and cause one of its components, usually C3, to bind to the bacterium and act as a ligand for its phagocytosis by macrophages. Complement binding induced by the antigen-antibody complex may also cause foreign cells to lyse.
The cell-mediated immune response: Cytotoxic T lymphocytes target and destroy transformed and virus-infected cells
When the TCR of a cytotoxic T lymphocyte recognizes and binds to an antigen-MHC I complex on the surface of a transformed or virus-infected cell, cytokines are released from the cell that cause it to proliferate. The cytotoxic T cells then secrete other cytokines (e.g., lymphokines, perforins, and fragmentins) that induce the cell to undergo apoptosis or to lyse (Fig. 13.8).
When an individual has been immunologically sensitized by exposure to antigen, subsequent exposure may lead not only to secondary response but also to tissue-damaging reactions called hypersensitivity reactions. Such reactions are observed in sensitized humans, following insect bites or injections of penicillin. One common type of hypersensitivity reaction is the allergic reaction. Certain aspects of a hypersensitivity reaction are caused by the antibody-induced discharge of mast cell granules. These granules contain histamine that accounts for the distressing features of hypersensitivity reactions. Eosinophils are attracted to the site of mast cell degranulation, where they neutralize the effects of histamine. Thus, eosinophils are frequently seen in connective tissue at allergic or other hypersensitivity reaction sites.
Suppressor/cytotoxic T lymphocytes turn off the immune response
Suppressor/cytotoxic CD8+, CD45RA+ T lymphocytes diminish or suppress antibody formation by B cells. They also downregulate the ability of cytotoxic T lymphocytes to provide a cell-mediated immune response and participate in delayed hypersensitivity reactions (allergic reactions). Suppressor/cytotoxic T lymphocytes may also function in the regulation of erythroid cell maturation in bone marrow.
fragmentins activation of NK cell
Fc receptors tumor antigen activation of apoptosis perforins
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