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B cell tolerance--how to make it and how to break it.
Journal article

B cell tolerance--how to make it and how to break it.

  • Melchers F Department of Cell Biology, Biozentrum, University of Basel, Switzerland. fritz.melchers@unibas.ch
  • Rolink AR
  • 2006-05-27
Published in:
  • Current topics in microbiology and immunology. - 2006
Animals
Autoimmune Diseases
B-Lymphocytes
Humans
Immune Tolerance
Immunoglobulin M
Receptors, Antigen, B-Cell
T-Lymphocytes
Toll-Like Receptors
English A series of checkpoints for antigen receptor fitness and specificity during B cell development ensures the elimination or anergy of primary, high-avidity-autoantigen-reactive B cells. Defects in genes encoding molecules with which this purging of the original B cell repertoires is achieved may break this B cell tolerance, allowing the development of B cell- and autoantibody-mediated immune diseases. Furthermore, whenever tolerance of helper T cells to a part of an autoantigen is broken, a T cell-dependent germinal center-type response of the remaining low--or no--autoreactive B cells is activated. It induces longevity of these B cells, and expression of AiD, which effects Ig class switching and IgV-region hypermutation. The development of V-region-mutant B cells and the selections of high-avidity-autoantigen-reactive antibodies producing B cells by autoantigens from them, again, can lead to the development and propagation of autoimmune diseases such as lupus erythematosus or chronic inflammatory rheumatoid arthritis by the autoantibody BcR-expressing B cells and their secreted autoantibodies.
Language
  • English
Open access status
closed
Identifiers
Persistent URL
https://sonar.ch/global/documents/165152
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