AI Article Synopsis
- B cells play a key role in the development of systemic lupus erythematosus (SLE) by becoming activated in response to immune signals, which disrupts normal tolerance to the body's own nuclear antigens.
- The review examines how both B cell receptors and Toll-like receptors contribute to this activation, and highlights the various roles B cells play, whether through producing autoantibodies or other immune functions.
- Therapeutic strategies targeting B cells in SLE have experienced mixed results, but recent studies suggest that better understanding of immune mechanisms may improve treatment outcomes in the future.
Article Abstract
B cells exert a prominent contribution to the pathogenesis of systemic lupus erythematosus (SLE). Here, we review the immune mechanisms underlying autoreactive B cell activation in SLE, focusing on how B cell receptor and Toll-like receptor signals integrate to drive breaks in tolerance to nuclear antigens. In addition, we discuss autoantibody-dependent and autoantibody-independent B cell effector functions during lupus pathogenesis. Finally, we address efforts to target B cells therapeutically in human SLE. Despite initial disappointing clinical trials testing B cell depletion in lupus, more recent studies show promise, emphasizing how greater understanding of underlying immune mechanisms can yield clinical benefits.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8357318 | PMC |
| http://dx.doi.org/10.1016/j.rdc.2021.04.006 | DOI Listing |
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