期刊
JOURNAL OF IMMUNOLOGY
卷 176, 期 2, 页码 984-990出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.176.2.984
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- NCI NIH HHS [CA88059, CA83130] Funding Source: Medline
CD4(+) T cells naturally expressing CD25 molecules (natural T regulatory cells (Tregs)) have a role in maintaining self tolerance and in regulating responses to infectious agents, transplantation Ags, and tumor Ags. CD4(+) Tregs induced from CD4(+)CD25(-) precursors (induced Tregs) also regulate immune responses in the periphery. However, which of these Tregs is a major impediment in generating antitumor CTL responses is not clear. We show that although the CD4(+)CD25(+) subsets isolated from peripheral blood-derived lymphocytes do suppress the proliferation of CD4(+)CD25(-) effector T cells, they do not suppress the activation and expansion of the self but melanoma-associated, melanoma Ag-reactive T cell 1 (MART-1)(27-35)-specific CD8(+) T cells stimulated by the respective peptide-loaded matured dendritic cells in vitro. The CD4+CD25- counterparts, in contrast, lead to the generation of CD25(+) glucocorticoid-inducible TNFR+-Forkhead/winged helix transcription factor(+) populations and efficiently suppress the activation and expansion of the MART-1(27-35) epitope-specific CTLs. Our data suggest that when CTL precursors are optimally stimulated, natural Tregs are not a formidable constraint toward generating a robust antitumor CTL response, but induced Tregs could be.
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