REVIEW - Infections, B cell receptor activation and autoimmunity

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Autoimmun Rev. 2007 Dec;7(2):109-13. Epub 2007 Mar 26.

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.

Division of Rheumatology, School of Medicine, Catholic University of

the Sacred Heart-CIC Via Moscati 31, Rome, 00168 Italy.

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.

PMID: 18035319

http://www.ncbi.nlm.nih.gov/sites/entrez?Db=pubmed & Cmd=ShowDetailView & TermToSear\

ch=18035319

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Not an MD