Authors
Alan D Salama, Tanuja Chitnis, Jaime Imitola, Mohammed Javeed I Ansari, Hisaya Akiba, Fumihiko Tushima, Miyuki Azuma, Hideo Yagita, Mohamed H Sayegh, Samia J Khoury
Publication date
2003/7/7
Journal
The Journal of experimental medicine
Volume
198
Issue
1
Pages
71-78
Publisher
Rockefeller University Press
Description
Experimental autoimmune encephalomyelitis (EAE) is mediated by autoantigen-specific T cells dependent on critical costimulatory signals for their full activation and regulation. We report that the programmed death-1 (PD-1) costimulatory pathway plays a critical role in regulating peripheral tolerance in murine EAE and appears to be a major contributor to the resistance of disease induction in CD28-deficient mice. After immunization with myelin oligodendrocyte glycoprotein (MOG) there was a progressive increase in expression of PD-1 and its ligand PD-L1 but not PD-L2 within the central nervous system (CNS) of mice with EAE, peaking after 3 wk. In both wild-type (WT) and CD28-deficient mice, PD-1 blockade resulted in accelerated and more severe disease with increased CNS lymphocyte infiltration. Worsening of disease after PD-1 blockade was associated with a heightened autoimmune response to MOG …
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Scholar articles
AD Salama, T Chitnis, J Imitola, MJI Ansari, H Akiba… - The Journal of experimental medicine, 2003
AD Salama, T Chitnis, J Imitola, MJI Ansari, H Akiba… - JOURNAL OF EXPERIMENTAL MEDICINE, 2003