Abstract
Dysregulation of the IL-23/Th17 immune axis is a major driver of PsO. The A2AR is a key regulator of both immunity and inflammation. Recently, we described a unique means to enhance A2AR function through a small molecule that acts as a positive allosteric modulator (PAM) of the receptor. The PAM has no intrinsic activity at the A2AR but enhances endogenous adenosine-mediated A2AR function. The PAM alters the function of both mouse and human monocytes, pDCs, cDCs, γδT and CD4+ T cells as well as human epidermal keratinocytes to reduce expression/production of key cytokine mediators implicated in PsO.
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