Article ID: b18-00261
Recent studies suggested that excessive Th1/17 cells concomitant with regulatory T cell deficiency might play important roles in Crohn’s disease. Anti-CD52 mAb, which aims on CD52 antigen on mature immunocytes, has both T cell depletion and immunosuppressive activities. In this study, we evaluated the therapeutic effects and possible mechanisms of anti-CD52 treatment on interleukin-10 deficient mouse. Anti-mouse CD52 mAb was administered to C3H.IL-10-/- mice intraperitoneally 20μg per week for 2 weeks. The disease activity index, body weight, the histological grading of colitis, and levels of TNF-α, IFN-γ, IL-17 and IL-6 in colon were quantified after treatment. In addition, CD25, Foxp3 and TGF-β gene as well as the percentage of CD25+Foxp3+ T cells in colon were also measured. The severity of colitis in IL-10-/- mice was significantly decreased by the treatment, with improvement of colon histological grade. The treatment also decreased the TNF-α, IFN-γ, IL-17 and IL-6 levels in colon. Furthermore, the treatment up-regulated the mRNA expression of CD25, Foxp3 and TGF-β gene as well as the percentage of CD25+Foxp3+ T cells in colon LPMCs of IL-10-/- mice. Our data might indicate that anti-CD52 treatment could ameliorate the colitis of C3H.IL-10-/- mice and it might be related to the suppression of Th1/17 related inflammation and the promotion of regulatory T cell differentiation. Thus, our data reveals that anti-CD52 treatment may hold potential for clinical applications for Crohn’s disease treatment.
