Deficient Arginase II Expression without Alteration in Arginase I Expression Attenuated Experimental Autoimmune Encephalomyelitis in Mice.

In conclusion, Arg II was identified as a factor promoting EAE likely via an Arg I-independent mechanism. Arg II may promote EAE by enhancing DC production of Th17-differentiating cytokines. Specific inhibition of Arg II could be a potential therapy for MS. This article is protected by copyright. All rights reserved.
PMID: 29574762 [PubMed - as supplied by publisher]

Source: Immunology - March 25, 2018 Category: Allergy & Immunology Authors: Choudry M, Tang X, Santorian T, Wasnik S, Xiao J, Xing W, Lau KW, Mohan S, Baylink DJ, Qin X Tags: Immunology Source Type: research