Inhibitory KIR3DL1 alleles are associated with psoriasis

Funding sources: W.L. acknowledges support from National Institutes of Health (NIH) grants R01AR065174 and K08AR057763. A.M.B. acknowledges support from NIH grant 2R01AR050266. This project has been funded in whole or in part with federal funds from the Frederick National Laboratory for Cancer Research, under contract no. HHSN261200800001E. This research was supported in part by the Intramural Research Program of the NIH, Frederick National Lab, Center for Cancer Research. Conflicts of interest: none declared. Dear Editor, Genetic association studies have implicated over 40 genetic loci in the pathogenesis of psoriasis, with the largest signal observed at the major histocompatibility complex (MHC) class I locus for human leucocyte antigen (HLA)‐C. However, recent data also suggest a lesser but significant pathogenic role for HLA‐B.1 2 Although both of these molecules participate in adaptive immunity through antigen presentation, they can also regulate the innate immune response through interaction with killer cell immunoglobulin‐like receptors (KIRs) expressed on the surface of both natural killer cells and a subset of T cells. KIRs form a family of receptors encoded by a cluster of 14 genes on chromosome 19q13·4. They may encode activating or inhibitory receptors that bind the Bw4 motif on HLA‐B or the C1/C2 motif on HLA‐C.3