Killer‐Cell Immunoglobulin‐Like Receptors ( KIR ) and HLA ‐Class I Heavy Chains in Ankylosing Spondylitis

Postmarketing Phase IVHLA‐B 27 (B27) interactions with the killer‐cell immunoglobulin‐like receptors ( KIR ) have been implicated in the pathogenesis of ankylosing spondylitis ( AS ), with consistent differences among populations. KIR3DL 1 and possibly KIR3DS 1 interact with classical B 27, whereas KIR3DL 2 binds B 27 heavy chain dimers. The aim of this review is to summarize data from recent studies performed in our laboratory and from the literature, which provide support for a possible role of KIR3DL2/B 27 dimer interactions in the pathogenesis of AS . Recent studies in cells from AS patients and from health controls carrying the predisposing B *2705 and the nonpredisposing B *2709 haplotypes, have shown a higher percentage of positive cells and a higher surface expression of KIR3DL 2 receptors on natural killer ( NK ) and CD 4+ T cells in B *2705 AS patients compared with B *2705, B *2709 and B 27‐negative healthy controls. Increased expression of HC 10‐reactive molecules on AS monocytes was seen, supporting the possible role of the KIR3DL2/B 27 2 pair in the pathogenesis of AS . These results underline the importance of NK cells and innate immunity, and of CD 4+ T cells in the inflammatory pathogenesis of AS .