期刊
JOURNAL OF IMMUNOLOGY
卷 181, 期 12, 页码 8209-8213出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.181.12.8209
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资金
- Intramural NIH HHS [ZIA AI000224-28] Funding Source: Medline
CD4(+) T cells from the TCR transgenic TxA23 mouse recognize a peptide from the H/K-ATPase alpha-chain. When TxA23 CD4(+) thymocytes are differentiated into Th1, Th2, and Th17 lines, all three subpopulations induced autoimmune gastritis (AIG) upon transfer into nu/nu recipients. The induction of AIG by naive T cells or by Th1 or Th2 cell lines could be prevented by the cotransfer of polyclonal Foxp3(+) T regulatory cells (nTreg), whereas Th17-induced AIG was resistant to suppression. We compared the capacity of different types of Treg to suppress Th17-mediated AIG. Cotransfer of either nTreg or polyclonal TGF beta-induced Treg (iTreg) did not prevent AIG, while cotransfier of TGF beta-induced Ag-specific TxA23 iTreg completely prevented the development of disease. Ag-specific iTreg were able to suppress Th17-mediated disease when injected 6 days after the Th17 effectors. The implications of these results for the use of Treg for the cellular biotherapy of autoimmune disease are discussed. The Journal of Immunology, 2008, 181: 8209-8213.
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