035 Blocking IL-7, but not TLR7, signaling prevents the development of lupus-like autoimmunity in mice

Abstract

Systemic lupus erythematosus (SLE) is a female-biased multisystem inflammatory disease with substantial morbidity and mortality and limited treatment options. Our lab previously found that VGLL3, a putative transcription co-factor with increased activity in female cells, can drive lupus-like systemic inflammation when overexpressed in mouse epidermis under the K5 promoter. IL-7 signaling was found to be elevated in the skin of lupus patients and K5-Vgll3+ mice alike. Our current results demonstrate that deleting peripheral Il7r in these mice prevents the development of disease phenotype, with amelioration of dermatitis, splenomegaly, lymphadenopathy, and kidney damage.