期刊
PLOS ONE
卷 12, 期 7, 页码 -出版社
PUBLIC LIBRARY SCIENCE
DOI: 10.1371/journal.pone.0180688
关键词
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资金
- USA National Institutes of Health National Institute for General Medical Sciences [GM082916]
- Hartwell Foundation
- USA National Institutes of Health Institute for Allergy and Infectious Disease [F32A1114109]
- Case Comprehensive Cancer Center [P30CA043703]
- Cytometry & Imaging Microscopy Core Facility of the Case Comprehensive Cancer Center
While Toll-like receptors (TLRs) represent one of the best characterized innate immune pathways, evidence suggests that TLRs are not restricted to innate leukocytes and some epithelial cells, but are also expressed in T cells. Specifically, published evidence focusing on FoxP3 + regulatory T cells demonstrate that they express functional TLR2, which is already known among the TLR family for its association with immune suppression; however, little is known about the relationship between T cell-intrinsic TLR2 binding and cytokine production, T cell differentiation, or T cell receptor (TCR) stimulation. Here, we demonstrate that TCR and TLR2 co-stimulation provides a T cell-intrinsic signal which generates a dramatic, synergistic cytokine response dominated by IL-10. Importantly, the response was not seen in either CD4(+) CD25(+) or CD4(+) FoxP3(+) Tregs, yet resulted in the expansion of a suppressive CD4(+) CD25(+) CD62L(-) CD44(+) CD45Rb hi effector/memory T cell subset not typically associated with immune inhibition. This study reveals the striking ability of a prototypical innate immune receptor to trigger a potent and suppressive IL-10 response in effector/memory T cells, supporting the notion that TLR2 is a co-regulatory receptor on T cells.
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