do not necessarily upregulate IL-17A and downregulate IL-17F production upon activation [46]. Notably, the observed effects of CREMα on IL-2 and IL-17A cytokine production in humans are also observed in transgenic mice with T cell-specific CREMα overexpression (under control of the cd2 promoter). These mice have decreased IL-2 and increased IL-17A levels and are more prone to develop signs of autoimmunity (including lymphadenopathy, elevated IL-17 production, and higher autoantibody titers against double-stranded DNA) when an additional genetic deletion of the cd95 gene is present [52]. These data support the idea of CREMα as an independent promoter of the ‘autoimmune phenotype’.
