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. 2015 Jul:61:9-16.
doi: 10.1016/j.jaut.2015.04.007. Epub 2015 May 29.

Deleting the BAFF receptor TACI protects against systemic lupus erythematosus without extensive reduction of B cell numbers

William A Figgett  1 , Devy Deliyanti  2 , Kirsten A Fairfax  3 , Pin Shie Quah  2 , Jennifer L Wilkinson-Berka  2 , Fabienne Mackay  2
Affiliations

Deleting the BAFF receptor TACI protects against systemic lupus erythematosus without extensive reduction of B cell numbers

William A Figgett et al. J Autoimmun. 2015 Jul.

Abstract

B cell-activating factor of the TNF family (BAFF) is an essential B cell survival factor. However, high levels of BAFF promote systemic lupus erythematosus (SLE) in mice and humans. Belimumab (anti-human BAFF) limits B cell survival and is approved for use in patients with SLE. Surprisingly, the efficacy of rituximab (anti-human CD20) in SLE remains controversial, despite depleting B cells more potently than belimumab. This raises the question of whether B cell depletion is really the mechanism of action of belimumab. In BAFF transgenic mice, SLE development is T cell-independent but relies on innate activation of B cells via TLRs, and TLR expression is modulated by the BAFF receptor TACI. Here, we show that loss of TACI on B cells protected against BAFF-mediated autoimmune manifestations while preserving B cells, suggesting that loss of BAFF signaling through TACI rather than loss of B cells may underpin the effect of belimumab in the clinic. Therefore, B cell-sparing blockade of TACI may offer a more specific and safer therapeutic alternative to broad B cell depletion in SLE.

Keywords: Autoantibodies; BAFF; Lupus nephritis; Systemic lupus erythematosus; TACI; TLR7.

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