Fig. 6From: Dual-specificity phosphatases 22-deficient T cells contribute to the pathogenesis of ankylosing spondylitisSchematic diagram of the correlation of DUSPs and ankylosing spondylitis. The mRNA levels of DUSP4, DUSP5, DUSP6, DUSP7, and DUSP14 were increased in peripheral blood T cells from ankylosing spondylitis (AS) patients, whereas the mRNA levels of DUSP22 were decreased. Downregulation of the DUSP22 protein in T cells of AS patients was concomitant to the induction of the proinflammatory cytokines TNF-α, IL-17A, and IFN-γ. DUSP22 downregulation was correlated with the values/levels of ESR, CRP, BASDAI, TNF-α, IL-17A, and IFN-γ of AS patients. Consistently, DUSP22 knockout (KO) mice spontaneously developed AS-like symptoms with induction of TNF-α, IL-17A, and IFN-γ. It is unclear whether IFN-γ contributes to the pathogenesis of AS. In addition, the mRNA levels of DUSP4, DUSP5, DUSP6, DUSP7, and DUSP14 were modestly correlated with TNF-α mRNA levels in the T cells of AS patients. The roles of DUSP4, DUSP5, DUSP6, DUSP7, and DUSP14 in the pathogenesis of AS are unclear. These findings suggest that DUSP22 downregulation in T cells plays a critical role in the pathogenesis of AS. ESR, erythrocyte sedimentation rate; CRP, C-reactive protein; BASDAI, Bath Ankylosing Spondylitis Disease Activity IndexBack to article page