Volume 14, Issue 3 (9-2012)                   yafte 2012, 14(3): 45-57 | Back to browse issues page

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Abstract:   (10362 Views)
Background : Ankylosing spondylitis (AS) represents a progressive and debilitating disease that affects approximately 0.9% worldwide. So far the precise mechanisms underlying the initiation and progression of AS is still unclear. Linkage between HLA-B27 and AS remains the strongest association between a human leukocyte antigen (HLA) class I molecule and disease. Despite intensive research, the pathogenic role of this gene and its product has not yet been resolved. Non-HLA-B27 genes exist that also seem to be involved in disease etiology. The killer immunoglobulin-like receptor (KIR) gene cluster is located on chromosome 19q13.4 in the leukocyte receptor complex. The KIR genes encode a group of proteins that are expressed on natural killer (NK) cells and in some T cells. KIR proteins act as receptors that recognize HLA class I molecules and are directly involved in the activation and inhibition of NK cells. KIRs and their HLA class I ligands contribute to the pathogenesis of diverse kinds of autoimmune diseases. The genetic imbalance of inhibitory and activating KIRs may be the key factor, which influences the pathogenesis of AS. However, the role of balance between inhibitory and activating KIRs in determining susceptibility to AS a topic of debatable. This review summarizes the major features of these genes and discusses how they may be involved in AS pathogenesis.
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Type of Study: Research |
Received: 2012/09/17 | Accepted: 2012/11/12 | Published: 2012/09/15

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