Journal
JOURNAL OF LEUKOCYTE BIOLOGY
Volume 92, Issue 5, Pages 987-997Publisher
OXFORD UNIV PRESS
DOI: 10.1189/jlb.0911465
Keywords
MDSC; cancer; immunosuppression
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Funding
- U.S. National Institutes of Health [R01 CA104926]
- Cancer Biology Training grant [T32 CA009213]
- AZ Cancer Center [CA023074]
- Tee Up for Tots
- PANDA Funds
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MDSCs and Tregs play an essential role in the immunosuppressive networks that contribute to tumor-immune evasion. The mechanisms by which tumors promote the expansion and/or function of these suppressive cells and the cross-talk between MDSC and Treg remain incompletely defined. Previous reports have suggested that MDSC may contribute to Treg induction in cancer. Herein, we provide evidence that tumor-induced gr-MDSCs, endowed with the potential of suppressing conventional T Lc, surprisingly impair TGF-beta 1-mediated generation of CD4(+)CD25(+)FoxP3(+) iTregs. Furthermore, gr-MDSCs impede the proliferation of nTregs without, however, affecting FoxP3 expression. Suppression of iTreg differentiation from naive CD4(+) cells by gr-MDSC occurs early in the polarization process, requires inhibition of early T cell activation, and depends on ROS and IDO but does not require arginase 1, iNOS, NO, cystine/cysteine depletion, PD-1 and PD-L1 signaling, or COX-2. These findings thus indicate that gr-MDSCs from TB hosts have the unanticipated ability to restrict immunosuppressive Tregs. J. Leukoc. Biol. 92: 987-997; 2012.
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