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Proc Natl Acad Sci U S A. 2012 Aug 7;109(32):13064-9. doi: 10.1073/pnas.1120585109. Epub 2012 Jul 23.

Toll-like receptor 4 signaling in T cells promotes autoimmune inflammation.

Author information

1
Department of Immunology and Center for Inflammation and Cancer, MD Anderson Cancer Center, Houston, TX 77054, USA.

Abstract

Toll-like receptors (TLRs) are critical components of innate immunity and function as rapid pathogen sensors. TLR4 is expressed on CD4(+) T cells as well, the functional significance of which is unclear. In this study, we analyzed the function of TLR4 in T cells but did not find a role in promoting T helper (Th) cell polarization. Instead, TLR4 ligation enhanced both CD4(+) T-cell proliferation and survival in vitro. Using the experimental autoimmune encephalomyelitis (EAE) model, we found that the loss of TLR4 solely in CD4(+) T cells almost completely abrogated disease symptoms, mainly through blunted Th17 and, to a lesser degree, Th1 responses. Moreover, Tlr4(-/-) γδ T cells were defective in IL-17 and IFN-γ production following EAE induction. This study supports an important role of this innate receptor in the direct regulation of T-cell activation and survival during autoimmune inflammation.

PMID:
22826216
PMCID:
PMC3420161
DOI:
10.1073/pnas.1120585109
[Indexed for MEDLINE]
Free PMC Article

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