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We read with great interest the article on cortistatin (CST) treatment for collagen-induced arthritis by Gonzalez-Rey et al.(1) They reported that CST could decrease the frequency and reduce the severity of collagen-induced arthritis. In addition, they reported that CST treatment could induce the generation of regulatory T (Treg) cell in periphery. This is important, as little is presently known about th...
We read with great interest the article on cortistatin (CST) treatment for collagen-induced arthritis by Gonzalez-Rey et al.(1) They reported that CST could decrease the frequency and reduce the severity of collagen-induced arthritis. In addition, they reported that CST treatment could induce the generation of regulatory T (Treg) cell in periphery. This is important, as little is presently known about the factors and mechanisms controlling Treg cell expansion in periphery.(2) Treg cells have emerged as key players in the development of tolerance to autoantigens as well as to foreign antigens.(3) Until now, few investigations explored the immunomodulatory role of cortistatin in transplantation. We would like to share the results in our study on CST treatment for grafts rejection in a skin transplantation model. In our study, we find that CST treatment can induce more than two-fold increase of CD25+CD4+ T cells in the CD4+T cells of recipients (fig 1), up-regulate the expression of Foxp3, induce hyporesponsiveness to fully allogeneic antigens and prolong survival time of allogeneic skin grafts. Traditional immunosuppressive drugs, such as FK506 and cyclosporin A (CsA), treatment may be accompanied by several side effects, including interfering with the generation of Treg cell.(4) Thus, the establishment of additional strategies for immunosuppression of allograft rejection to minimize complications is desirable. AS an effectively suppressive neuropeptide in transplant rejection and one of the endogenous factors controlling the peripheral expansion of the Treg cells, CST may become a new modality in controlling allograft rejection.
Figure 1. The percentages of CD25+CD4+T cells in the CD4+T lymphocytes of skin transplant recipients. T lymphocytes enriched from splenocytes of BALB/c recipients treated with PBS, various doses of CST(0.02, 0.2 or 2 mg/kg) were isolated on day 7 post-transplantation and stained with three-color fluorescence labeled antibodies against mouse CD3, CD4 and CD25. The percentages of CD25+CD4+T cell were analyzed by flow cytometry. Recipients treated with PBS were acted as control group. A representative experiment of three is shown.
1. Gonzalez-Rey E, Chorny A, Del Moral RG, Varela N, Delgado M. Therapeutic effect of cortistatin on experimental arthritis by downregulating inflammatory and Th1 responses. Ann Rheum Dis 2007;66:582-588.
2. Sykes M. Immune tolerance: mechanisms and application in clinical transplantation. Journal of internal medicine 2007;262:288-310.
3. Kang SM, Tang Q, Bluestone JA. CD4+CD25+ regulatory T cells in transplantation: progress, challenges and prospects. Am J Transplant 2007;7:1457-1463.
4. Lim DG, Joe IY, Park YH, Chang SH, Wee YM, Han DJ, et al. Effect of immunosuppressants on the expansion and function of naturally occurring regulatory T cells. Transplant immunology 2007;18:94-100.