Abstract
TGF-β and Foxp3 expressions are crucial for the induction and functional activity of CD4+Foxp3+ regulatory T (iTreg) cells. Here, we demonstrate that although TGF-β-primed CD8+ cells display much lower Foxp3 expression, their suppressive capacity is equivalent to that of CD4+ iTreg cells, and both Foxp3- and Foxp3+ CD8+ subsets have suppressive activities in vitro and in vivo. CD8+Foxp3- iTreg cells produce little IFN-γ but almost no IL-2, and display a typical anergic phenotype. Among phenotypic markers expressed in CD8+Foxp3- cells, we identify CD103 expression particularly crucial for the generation and function of this subset. Moreover, IL-10 and TGF-β signals rather than cytotoxicity mediate the suppressive effect of this novel Treg population. Therefore, TGF-β can induce both CD8+Foxp3- and CD8+Foxp3 + iTreg subsets, which may represent the unique immunoregulatory means to treat autoimmune and inflammatory diseases.
Original language | English (US) |
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Pages (from-to) | 81-92 |
Number of pages | 12 |
Journal | Journal of Molecular Cell Biology |
Volume | 6 |
Issue number | 1 |
DOIs | |
State | Published - Feb 2014 |
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Genetics
- Cell Biology