Suppression of autoimmunity and organ pathology in lupus‐prone mice upon inhibition of calcium/calmodulin‐dependent protein kinase type IV

Abstract

We conclude that suppression of CaMKIV mitigates disease development in lupus-prone mice by suppressing cytokine production and costimulatory molecule expression. Specific silencing of CAMK4 in human T cells results in similar suppression of IFNγ production. Our data justify the development of small-molecule CaMKIV inhibitors for the treatment of patients with SLE.