Accelerated course of experimental autoimmune encephalomyelitis in PD-1-deficient central nervous system myelin mutants.

ABSTRACT: It is assumed that the onset and course of autoimmune inflammatory central nervous system (CNS) disorders (eg, multiple sclerosis) are influenced by factors that afflict immune regulation as well as CNS vulnerability. We challenged this concept experimentally by investigating how genetic alterations that affect myelin (primary oligodendrocyte damage in PLPtg mice) and/or T-cell regulation (deficiency of PD-1) influence both the onset and course of an experimental autoimmune CNS inflammatory disease [MOG(35-55)-induced experimental autoimmune encephalomyelitis (EAE)]. We observed that double pathology was associated with a significantly earlier onset of disease, a slight increase in the neurological score, an increase in the number of infiltrating cells, and enhanced axonal degeneration com

SUBMITTER: Kroner A 

PROVIDER: S-EPMC2684193 | biostudies-literature | 2009 Jun

REPOSITORIES: biostudies-literature