Abstract:OBJECTIVE: To explore the expression diversification of CD4+CD25+CD127low regulatory T (Treg) cells and Foxp3 mRNA in the peripheral blood of children with aplastic anemia after the treatment with cyclosporine. METHODS: Fifty children with chronic aplastic anemia were enrolled, among whom 30 received cyclosporine treatment (cyclosporine group) and 20 were treated with conventional methods (conventional group). Twenty healthy children were enrolled as the control group. The expression of CD4+CD25+CD127low Treg cells was detected by flow cytometry. The expression of Foxp3 mRNA was detected by real-time Q-PCR. RESULTS: The expressions of Foxp3 mRNA and CD4+CD25+CD127lowTreg cells showed no significant difference between the cyclosporine and the control groups 6 months after treatment. On the contrary, there were significantly lower expressions of both in the conventional group than in the control group (P<0.05). Meanwhile, the cyclosporine group had significantly higher expressions of Foxp3 mRNA and CD4+CD25+CD127low Treg cells than the conventional group (P<0.05). CONCLUSIONS: The expressions of CD4+CD25+CD127low Treg cells and Foxp3 mRNA in children with aplastic anemia increase after cyclosporine treatment.
WANG Xi-Ge,WANG Meng,LIU Song et al. Effect of cyclosporine on regulatory T cells and Foxp3 in the peripheral blood of children with chronic aplastic anemia[J]. CJCP, 2011, 13(12): 936-939.
[11]Fiedler B, Wollert KC. Inter ference of antihypertrophic molecules and signaling pathways with the Ca2+-calcineurin-NFAT cascade in cardiacmy ocytes[J]. Cardiovasc Res, 2004, 63(3): 450-457.
[12]Bayer AL, Yu A, Malek TR. Function of the IL-2R for thymic and peripheral CD4+ CD25+ Foxp3+ T regulatory cells[J]. J Immunol, 2007, 178(7): 4062-4071.
[13]Lutsiak ME, Semnani RT, De Pascalis R, Kashmiri SV, Schlom J, Sabzevari H. Inhibition of CD4+CD25+ T regulatory cell function implicated in enhanced immune response by low-dose cyclophosphamide[J]. Blood, 2005, 105(7): 2862-2868.
[14]Godfrey WR, Spoden DJ, Ge YG, Baker SR, Liu B, Levine BL, et al.Cord blood CD4+CD25+ derived T regulatory cells linesexpress FOXP3 protein and manifest potent suppressor function[J]. Blood, 2005, 105(2): 750-758.
[15]Fontenot JD, Gavin MA, Rudensky AY. Foxp3 programs the development and function of CD4+CD25+ regulatory T cells[J]. Nax Immunol, 2003, 4(4): 330-336.
[16]Khattri R, Cox T, Yasayko SA, Ramsdell F. An essential role for scurfin in CD4+CD25+T regulatory cells[J]. Nat Immunol, 2003, 4(4): 337-342.
[17]Yagi H, Nomura T, Nakamura K, Yamazaki S, Kitawaki T, Hori S, et al. Crucial role of FOXP3 in the development and function of human CD25+CD4+regulatory T cells[J]. Int Immunol, 2004, 16(11): 1643-1656.
[18]Bacchetta R, Passerini L, Gambineri E, Dai M, Allan SE, Perroni L, et al.Defective regulatory and effector T cell functions in patients with FOXP3 mutations[J]. J Clin Invest, 2006, 116(6): 1713-1722.
[19]Gambineri E, Torgerson TR, Ochs HD. Immune dysregulation, polyendocrinopathy, enteropathy, and X-linked inheritance(IPEX), a syndrome of systemic autoimmunity caused by mutations of FOXP3, a critical regulator of T-cell homeostasis[J]. Curr Opin Rheumatol, 2003, 15(4): 430-435.
[20]Unterberger C, Staples KJ, Smallie T, Williams L, Foxwell B, Schaefer A, et al. Role of STAT3 in glucocorticoid induced expression of thehuman IL-10 gene[J]. Mol Immunol, 2008, 45(11): 3230-3237.