Immunity, acquired

Author: Prof. Dr. med. Peter Altmeyer

Last updated on: 04.05.2024

Synonym(s)

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

Definition
This section has been translated automatically.

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
This section has been translated automatically.

Acquired immunity, also known as adaptive immunity, is primarily mediated by T and B lymphocytes. In the unimprinted state, each cell only carries receptors of a single specificity that differs from all other cells. The diversity of receptors required for this is achieved by a genetic mechanism that takes place during the development of these cells in the bone marrow and thymus. This creates 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") arise in each cell. During consecutive somatic selection, autoreactive lymphocytes are eliminated and relevant effector cells are selected.

Acquired immunity thus produces an immense number of receptor variations that are not combined on a single cell (see below immunity, innate).

The activation of antigen-presenting cells (APs) also requires various costimulatory factors. The induction of these factors only occurs after certain molecular patterns (see below PAMPs = pathogen associated molecular patterns) have been recognized by corresponding receptors (see below PRRs = pattern recognition receptors). This feedback loop in innate immunity appears to be eminently important in the avoidance of "immunity" to autoantigens and non-pathogenic environmental antigens.

Autoimmune diseases and allergies are probably due in part to disturbances in these mechanisms.

Antigen presentation on MHC-II molecules(MHC = "major histocompatibility complex") and the simultaneous expression of costimulatory 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 become recognizable through different effector mechanisms. For example, interferon-gamma-producing T helper cells of the TH1 type play a role in combating mycobacteria, interleukin-17-producing T helper cells in combating fungal infections and interleukin-4-producing T helper cells of the Th2 type in combating worm and parasite infections.

Activation-induced cell death (AICD - see apoptosis below) plays a key role in the termination of immune responses.

Note(s)
This section has been translated automatically.

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.