Immunology: BCR/ antibody genetic diversity mechanisms

somatic hypermutation (or SHM) is a cellular mechanism by which the immune system adapts to the new foreign elements that confront it (e.g. microbes), as seen during class switching. A major component of the process of affinity maturation, SHM diversifies B cell receptors used to recognize foreign elements (antigens) and allows the immune system to adapt its response to new threats during the lifetime of an organism.[1] Somatic hypermutation involves a programmed process of mutation affecting the variable regions of immunoglobulin genes. Unlike germline mutation, SHM affects only an organism's individual immune cells, and the mutations are not transmitted to the organism's offspring.[2]

Mistargeted somatic hypermutation is a likely mechanism in the development of B-cell lymphomas.[3

V(D)J recombination, less commonly known as somatic recombination, is the unique mechanism of genetic recombination that occurs only in developing lymphocytes during the early stages of T and B cell maturation. The process results in the highly diverse repertoire of antibodies/immunoglobulins (Igs) and T cell receptors (TCRs) found on B cells and T cells, respectively. The process is a defining feature of the adaptive immune system and its development was a key event in the evolution of jawed vertebrates.

V(D)J recombination occurs in the primary lymphoid organs (bone marrow for B cells and thymus for T cells) and in a nearly random fashion rearranges variable (V), joining (J), and in some cases, diversity (D) gene segments. The process ultimately results in novel amino acid sequences in the antigen-binding regions of Igs and TCRs that allow for the recognition of antigens from nearly all pathogens including bacteria, viruses, parasites, and worms as well as "altered self cells" as seen in cancer. The recognition can also be allergic in nature (e.g., to pollen or other allergens) or may be "autoreactive" and lead to autoimmunity.

In 1987, Susumu Tonegawa was awarded the Nobel Prize in Physiology or Medicine[1] "for his discovery of the genetic principle for generation of antibody diversity."[2]

Junctional diversity describes the DNA sequence variations introduced by the improper joining of gene segments during the process of V(D)J recombination. This process of V(D)J recombination has vital roles for the vertebrate immune system, as it is able to generate a huge repertoire of different T-cell receptor (TCR) and immunoglobulin molecules required for pathogen antigen recognition by T-cells and B cells, respectively. The inaccuracies of joining provided by junctional diversity is estimated to triple the diversity initially generated by these V(D)J recombinations1976 copyright act entitles fair use for non profit educational purposes and is extended by the DMCA

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