Chronic low-level expression of a molecule called 'thymic stromal lymphopoietin' (TSLP) can greatly alter the development of antibody-producing B cells, according to a paper published online in Nature Immunology.
David Rawlings and colleagues show that low amounts of TSLP produced by epithelial tissues in skin and lung can accelerate the premature release of B cells from the bone marrow, bypassing normal mechanisms that ensure these cells do not attack 'self' tissues. Additionally, TSLP triggers an increase in a particular subset of B cells called B-1b B cells. Mice expressing an inducible form of the gene encoding TSLP had abundant autoantibodies, which were synthesized by B-1b cells and B cells from the spleen. These mice displayed early symptoms of renal disease owing to damage caused by the accumulation of these autoantibodies in kidney tissues.
TSLP expression is linked to inflammatory allergic responses. The authors' findings suggest that chronic stimulation by TSLP might contribute to the development of antibody-mediated autoimmune diseases.
David J. Rawlings (University of Washington School of Medicine, Seattle, WA, USA)
Abstract available online.
(C) Nature Immunology press release.
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