Immunity, acquired

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.

1. Averbeck M et al (2007) Immunological basics of allergies. JDDG 5: 1015-1028