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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Infections, B cell receptor activation and autoimmunity: different check-point impairments lead to autoimmunity, clonal B cell expansion and fibrosis in different immunological settings.

B cells as autoantibody producing cells are major players in several autoimmune chronic inflammatory diseases (ACIDs). In some particular settings (i.e. Sjogren's syndrome, rheumatoid arthritis), the activated B cells could undergo malignant clonal expansion. Chronic infections by lymphotropic viruses (hepatitis C virus, Epstein Barr Virus, Herpes 6 and 8 viruses) could amplify the activation process by inducing antiapoptotic signals that lead to a longer survival of B cell subsets. This might then lead, through multiple oncogenic events, to benign first and malignant thereafter clonal B cell expansion. Understanding how the B cell are activated, how the B cell receptor activation can be maintained under control, which check-points could be deregulated and lead to a persistent activation is of crucial importance in benign and malignant diseases. The evidence suggests that the B cells faulty check-points are different in chronic lymphocytic leukaemia, in cryoglobulinemia, rheumatoid arthritis, systemic lupus erythematosus and systemic sclerosis.[1]

References

  1. Infections, B cell receptor activation and autoimmunity: different check-point impairments lead to autoimmunity, clonal B cell expansion and fibrosis in different immunological settings. Ferraccioli, G., Tolusso, B. Autoimmun. Rev (2007) [Pubmed]
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