AI-20 Defective BCR induced apoptosis linked to elevated levels of 9-o-acetylated sialyl gangliosides on B cells in lupus provides a potential therapeutic target for lupus

Abstract

Conclusions Our study demonstrates that B cell-intrinsic IFN-g receptor signals promote lupus pathogenesis via formation of spontaneous, autoimmune GCs. In addition, we have uncovered a novel cell-intrinsic program whereby IFN-g, together with BCR-, TLR-and/or CD40 signals, orchestrates B cell expression of the GC master transcription regulator BCL-6. Our combined findings suggest that this IFN-g signalling program may be a potential therapeutic target in SLE.