Non-classical MHC I-E negatively regulates macrophage activation and Th17 cell development in NOD mice.

Abstract:

:Transgenic expression of I-E molecules prevents diabetes in NOD mice. So far, the precise role of these non-classical MHC II molecules remains elusive. Here, we showed that transgenic expression of I-E(k) alpha 16 molecule in NOD mice selectively reduced Th17 cells in the thymus and pancreatic draining lymph nodes. The reduction in Th17 cells was associated with both attenuated IL-6 production and decreased activation of macrophages. Mechanistically, transgenic expression of the I-E molecule diminished expression of intracellular classical MHC II molecule and led to impaired TLR4-mediated signaling. In contrast to classical MHC II molecule, this non-classical MHC II molecule negatively regulates the inflammatory responses of macrophages. Altogether, our study reveals a novel regulatory role of I-E molecules in modulating inflammatory immune responses.

journal_name

Sci Rep

journal_title

Scientific reports

authors

Yang C,Guo N,Liu J,Yang J,Zhu K,Xiao H,Leng Q

doi

10.1038/srep12941

subject

Has Abstract

pub_date

2015-08-07 00:00:00

pages

12941

issn

2045-2322

pii

srep12941

journal_volume

5

pub_type

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