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Mechanisms of central tolerance for B cells

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TLDR
Mechanistic studies have begun to elucidate how divergent mechanisms that regulate tolerance are controlled, and single-cell antibody cloning has revealed defects of B cell central tolerance in human autoimmune diseases and in several human immunodeficiency diseases caused by single gene mutations.
Abstract
Receptor editing and apoptosis have crucial roles in promoting the central tolerance of B cells to self-antigens. Defects of these processes can result in autoimmunity or immunodeficiency disease in humans and mice.

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References
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Journal ArticleDOI

Somatic generation of antibody diversity

TL;DR: In the genome of a germ-line cell, the genetic information for an immunoglobulin polypeptide chain is contained in multiple gene segments scattered along a chromosome which are assembled by recombination which leads to the formation of a complete gene.
Journal ArticleDOI

Predominant Autoantibody Production by Early Human B Cell Precursors

TL;DR: The prevalence of self-reactive antibody formation and its regulation in human B cells is determined and a majority (55 to 75%) of all antibodies expressed by early immature B cells displayedSelf-reactivity, including polyreactive and anti-nuclear specificities.
Book ChapterDOI

Somatic Generation of Antibody Diversity1

TL;DR: In this paper, it was shown that an organism does not inherit even a single complete gene for antibody polypeptide chains, rather, the genetic information is transmitted in germline as no more than several hundred gene segments.
Journal ArticleDOI

C3d of Complement as a Molecular Adjuvant: Bridging Innate and Acquired Immunity

TL;DR: C3d is a molecular adjuvant of innate immunity that profoundly influences an acquired immune response and is found to differentiate between harmful and innocuous antigens.
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What are the mechanism of central tolerance?

The mechanisms of central tolerance for B cells include receptor editing and apoptosis. These processes help to promote tolerance to self-antigens and prevent autoimmunity or immunodeficiency diseases.