| Literature DB >> 24439904 |
Toru Koda1, Tatsusada Okuno2, Kazushiro Takata1, Josephe Archie Honorat1, Makoto Kinoshita3, Satoru Tada1, Masayuki Moriya4, Saburo Sakoda5, Hideki Mochizuki1, Atsushi Kumanogoh6, Yuji Nakatsuji7.
Abstract
Approximately one-third of patients with multiple sclerosis (MS) respond poorly to interferon-beta (IFN-β) therapy. Serum Sema4A is increased in MS patients, and those who have high Sema4A do not respond to IFN-β therapy. In this study, we investigated whether recombinant Sema4A abrogates the efficacy of IFN-β in mice with experimental autoimmune encephalomyelitis (EAE), an animal model of MS. Administration of Sema4A concurrently with IFN-β diminished the efficacy of IFN-β in EAE. These effects of Sema4A were attributed to promote Th1 and Th17 differentiation and to increase adhesive activation of T cells to endothelial cells, even in the presence of IFN-β.Entities:
Keywords: Experimental autoimmune encephalomyelitis (EAE); Interferon-beta (IFN-β); Multiple sclerosis (MS); Sema4A
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Year: 2014 PMID： 24439904 DOI： 10.1016/j.jneuroim.2013.12.014
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478