| Literature DB >> 29331804 |
Peng Zhang1, Chun-Lin Yang1, Ru-Tao Liu1, Heng Li1, Min Zhang1, Na Zhang1, Long-Tao Yue2, Cong-Cong Wang1, Ying-Chun Dou3, Rui-Sheng Duan4.
Abstract
Recent studies have demonstrated the important role of toll-like receptor 9 (TLR9) signalling in autoimmune diseases, but its role in myasthenia gravis (MG) has not been fully established. We show herein that blocking TLR9 signalling via the suppressive oligodeoxynucleotide (ODN) H154 alleviated the symptoms of experimental autoimmune myasthenia gravis (EAMG). With the downregulation of dendritic cells (DCs), TLR9 interruption reduced follicular helper T cells (Tfh) and germinal centre (GC) B cells, leading to decreased antibody production. In addition, TLR9+ B cells as well as total B cells in the spleen were inhibited by H154. These findings highlight the critical role of TLR9 in EAMG and suggest that the inhibition of the TLR9 pathway might be a potential pharmacological strategy for the treatment of myasthenia gravis.Entities:
Keywords: Experimental autoimmune myasthenia gravis; Follicular helper T cells; Germinal centre; Toll-like receptor 9
Mesh:
Substances:
Year: 2018 PMID: 29331804 DOI: 10.1016/j.molimm.2018.01.005
Source DB: PubMed Journal: Mol Immunol ISSN: 0161-5890 Impact factor: 4.407