An important role for B-cell activation factor and B cells in the pathogenesis of Sjogren's syndrome
PURPOSE OF REVIEW: This review provides an update on the specific, strong association between dysregulated production of the cytokine B-cell activation factor and Sjogren's syndrome, and offers new perspectives on potential pathogenic mechanisms. RECENT FINDINGS: Excess B-cell activation factor in mice triggers Sjogren's syndrome-like symptoms, and elevated serum B-cell activation factor in humans correlates with Sjogren's syndrome. B-cell activation factor is produced locally by activated monocytes, T cells and dendritic cells, and by epithelial cells and infiltrating B cells. Moreover, recent data in humans suggest that the innate immune system plays a role as an initiator of immune disorders in inflamed tissues. SUMMARY: Recent data have demonstrated the critical role of B-cell activation factor and B cells in the pathogenesis of Sjogren's syndrome, and its association with B lymphomas. Moreover, B-cell depleting treatments have confirmed the critical role of B cells in Sjogren's syndrome. Excess B-cell activation factor possibly corrupts B-cell tolerance and allows the emergence of self-reactive B cells that efficiently present antigen to T cells. In addition, B-cell activation factor may stimulate T-cell independent activation of B cells via Toll-like receptors; this recently identified mechanism could also play a separate, detrimental role in autoimmunity.
|Authors||Mackay, F.;Groom, J. R.;Tangye, S. G. :|
|Publisher Name||CURRENT OPINION IN RHEUMATOLOGY|
|URL link to publisher's version||http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17762603|
|OpenAccess link to author's accepted manuscript version||https://publications.gimr.garvan.org.au/open-access/2244|