Immunity, acquired

Synonym(s)

Acquired immune system; Acquired immunity; Adaptive immune system; Adaptive immunity; Specific immune system

Definition
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System of acquired, antigen-specific humoral (e.g. antibodies) and cellular defence mechanisms (e.g. lymphocytes) that are used in the defence against an invading pathogen. This form of reaction leads to immunological memory.

General information
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Acquired immunity is mainly mediated by T and B lymphocytes. Each cell carries only receptors of a single specificity, which is different from all other cells. The required diversity of receptors is achieved by a genetic mechanism that takes place in the bone marrow and thymus during the development of these cells. This results in the variable region of receptors, through which individual combinations of the so-called V, D and J gene segments (somatic recombination; V = "variety"; D = "diversity"; J = "joining") are created in each cell. In consecutive somatic selection, autoreactive lymphocytes are eliminated and relevant effector cells are selected.

The acquired immunity thus produces an immense number of receptor variations that are not combined on a single cell (see also Immunity, innate).

The activation of antigen-presenting cells (APs) also requires various costimulatory factors. These factors are induced only after the recognition of certain molecular patterns (see below PAMPs = pathogen associated molecular patterns) by corresponding receptors (see below PRRs = pattern recognition receptors). This feedback in innate immunity seems to be eminently important in the prevention of "immunity" against autoantigens and non-pathogenic environmental antigens.

Probably, autoimmune diseases and allergies are partly due to disturbances of these mechanisms.

The antigen presentation on MHC-II molecules(MHC = "major histocompatibility complex") and the simultaneous expression of costimulating molecules causes the activation and clonal proliferation of native CD4 T lymphocytes matching this antigen, which are necessary for the activation of specific B cells, specific CD8 T lymphocytes and macrophages. After activation of these cells, they are recognized by different effector mechanisms. Interferon-gamma-producing T-helper cells of the TH1 type play a role in the control of mycobacteria, interleukin-17 producing T-helper cells in the control of fungal infections, interleukin-4 producing T-helper cells of the Th2 type in the control of worm and parasite infections.

Activation-induced cell death (AICD - see apoptosis below) plays an important role in terminating immune responses.

Note(s)
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In addition to the "classical cells" of the immune system, tissue cell signals such as keratinocytes are becoming increasingly important in the local modulation of an immune response. Keratinocytes are e.g. one of the main sources of proinflammatory cytokines (e.g. IL-1-alpha, IL-1-beta, TNF-alpha; see below interleukins) and immunomodulating cytokines of the skin (IL-6, IL-12, IL-15, IL-18), which are also secreted in response to non-specific stimulation such as irritant traumatic or solar stimuli (see below UV-rays). Keratinocytes come into contact with lymphocytes via the expression of certain surface molecules (MHC II, ICAM-1, CD40). This is the initiation for the invasion of lymphocytes into the skin ( epidermotropy), a phenomenon that leads to the histological picture of cancellous bone disease in the eczema reaction.