The principal function of T and B lymphocytes is to support the immune defense mechanisms of the organism. To do this effectively, these cells have acquired the capability of recognizing and neutralizing a diverse array of 'nonself' antigenic epitopes. This diversity is inherent in the germline structure of the immune genes, which contain several different regions. These discrete regions of the immune genes undergo several recombinational steps and reassort-ment of multiple segments to express the primary immune protein products.

The reassortment of the immune regions is achieved via a cutting and pasting mechanism that draws its specificity from the presence of specific nucleotide signal sequences, modulation of the accessibility of the genomic regions necessary for recombination, developmentally regulated expression of enzymes that will catalyze the recombination and possibly monitoring mechanisms that will prevent nonlegitimate substrates from recombining. In order to ensure the fidelity of the reaction, all productive recombinational processes are limited to be intralocus. Nonetheless there is a baseline error rate in the recombination process and some interlocus recombinations are also catalyzed. When these recombinations are catalyzed between immune and nonimmune partners, the expression of the nonimmune gene is deregulated. If the nonimmune partner is a growth-stimulatory protein, the recombinational event can lead to a clonal expansion and eventually transformation of a lymphoid cell. As an extreme, these errors may also involve two nonimmune genes that contain nucleotide sequences that are similar to the recombinase signal sequences. Mistaken recombination of such partner genes may also be transforming if the two genes form a novel product with growth-stimulatory properties or if the expression of one of the growth-supporting partner genes is rendered lymphoid specific by the rearrangement. It is possible that the error-prone mechanisms by which these lymphoid-specific transformation events occur may also overlap with errors in other mechanisms that cause genetic instability and promote transformation of nonlymphoid tumors.

See also: Apoptosis; B lymphocyte repertoire; B lymphocyte differentiation; B lymphocytes; Bone marrow and hematopoiesis; Diversity, generation of; Genetic analysis at the molecular level; Immunoglobulin class switching; Immunoglobulin genes; Immunoglobulin structure; Leukemia; Lymphocytes; Lymphoma; T lymphocytes.

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