TLR4-RelA-miR-30a signal pathway regulates Th17 differentiation during experimental autoimmune encephalomyelitis development.

ABSTRACT:

Background

Toll-like receptor 4 (TLR4) is well known for activating the innate immune system; however, it is also highly expressed in adaptive immune cells, such as CD4⁺ T-helper 17 (Th17) cells, which play a key role in multiple sclerosis (MS) pathology. However, the function and governing mechanism of TLR4 in Th17 remain unclear.

Methods

The changes of TLR4 in CD4⁺ T cells from MS patients and experimental autoimmune encephalomyelitis (EAE) mice were tested. TLR4-deficient (TLR4^-/-) naïve T cells were induced in vitro and transferred into Rag1^-/- mice to measure Th17 differentiation and EAE pathology. DNA sequence analyses combining with deletion fragments and mutation analyses, chromatin immunoprecipitation (ChIP), and electroph

SUBMITTER: Qu X 

PROVIDER: S-EPMC6764145 | biostudies-literature | 2019 Sep

REPOSITORIES: biostudies-literature