Figure 4. Possible mechanism of the pathogenic role of KIR in SpA.

Figure 4

Possible mechanism of the pathogenic role of KIR in SpA.

Ankylosing Spondylitis: a) HLA-Bw4 (B27) can be recognized by KIR3DL1 conferring a strong inhibition and preventing the lysis of the cell b) Recognition of Bw4 (B27) by KIR3DL1 can be blocked (some viral peptides may cause the blockage of the inhibitory receptor 3DL1 or KIR3DL1 polymorphism can serve to alter the inhibitory response) and therefore, it is probable that a significant fraction of arthritrogenic ligands of B*27 might avoid their interaction with KIR3DL1 in the course of a microbial infection and influence the activation of activating NK receptors (KIR3DS1) and the subsequent progression to AS.

Psoriatic Arthritis: c) The susceptibility to PsA develop could be determined by the balance of activating and inhibitory KIR-HLA genotypes, where protective inhibitory effects against PsA appear to be restricted to KIR2DL. d) The combination of KIR2DS1 and/or KIR2DS2 with their HLA-Cw ligand group homozygosity (HLA-C2 and HLA-C1, respectively), where the inhibitory signal is missing, confers susceptibility to PsA. There are different intermediate combinations KIR-HLA and these genotypes could be classified by their ability to confer activation (susceptibility) or inhibition (protection).

From: KIR Genes and Their Role in Spondyloarthropathies

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