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IL‐21 Receptor Signaling Is Essential for BXSB‐Yaa SLE Pathogenesis

Interleukin‐21 (IL‐21) is a cytokine with pleiotropic actions on multiple lympho‐hematopoietic lineages. BXSB‐Yaa mice develop a severe form of a systemic lupus erythematosus (SLE)‐like disease caused by a mutation on the Y‐chromosome. We previously showed that BXSB‐Yaa mice express elevated levels of IL‐21, but the role of IL‐21 in BXSB‐Yaa disease pathogenesis was not determined. To investigate the importance of IL‐21 signaling in this disease, we crossed the BXSB‐Yaa mice onto the Il21r−/− background and monitored the mice for the characteristic BXSB‐Yaa autoimmune syndrome. A deficiency in IL‐21R resulted in the abrogation of all disease phenotypes, including abnormal splenic cell numbers and populations, Ig and anti‐nuclear antibody levels, kidney pathology, and morbidity/mortality. These results demonstrate that IL‐21 signaling is essential for the development of autoimmune disease in BXSB‐Yaa mice and suggest that IL‐21 may be a more broadly critical cytokine in SLE autoimmunity. This work was supported in part by a postdoctoral fellowship from the Arthritis Foundation (to J. Bubier), and NIH DK56597 and R21 DK074463 (to D. Roopenian) and the Intramural Research Program of the NIH, National Institute of Allergy and Infectious Diseases and National Heart, Lung and Blood Institute.