Epistatic interactions between killer immunoglobulin-like receptors and human leukocyte antigen ligands are associated with ankylosing spondylitis.

However, most of these interactions failed to reach significance after multiple testing correction and were not replicated in a semi-independent cohort of 14,844 healthy controls and 3,497 cases (cases are a subset of the Discovery cohort).

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We identified multiple nominally significant epistatic interactions between the genes encoding KIR s and their HLA ligands on both the subtype and allele level, suggesting that AS risk, as likely the case for many immune-mediated diseases, is modified by a mosaic of genetic effects that converge to influence the proinflammatory capacity of KIR expressing lymphocytes.

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