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Results of sibling and twin studies suggest that a substantial proportion of susceptibility to spondyloarthropathies arises from genes outside the human leukocyte antigen (HLA) region. There is increasing evidence that the pattern of cytokine secretion influences the course of spondyloarthropathies. A Th2 cytokine pattern (low tumor necrosis factor [TNF]-TNF-α low interferon [IFN]-γ, and high interleukin [IL]-10) dominates in the joints of reactive arthritis patients. For IL-10 and TNF-α a substantial proportion of cytokine production is under genetic control and influenced by genetic polymorphisms. Here we review the evidences for association of TNF-α and IL-10 polymorphisms with spondyloarthropathies and their functional implications.