| Literature DB >> 15265676 |
Roel C van der Veen1, Therese A Dietlin, Armine Karapetian, Steven M Holland, Florence M Hofman.
Abstract
The mechanism and regulation of immunosuppression by nitric oxide (NO) is unclear. Extra-cellular superoxide (EC-O2-) production by NADPH-oxidase (phox) may prevent NO-mediated suppression of T cell proliferation. p47(phox-/-) mice are resistant to experimental allergic encephalomyelitis (EAE), coinciding with enhanced splenic NO activity, but no causal link was established. Here, we demonstrate such link, since p47(phox-/-) mice developed severe EAE by adoptive transfer, but only if NO production during ex vivo donor cell reactivation was inhibited. EC-O2- production increased during cognate T cell reactivation, while inhibition of EC-O2- by exogenous superoxide dismutase enhanced NO activity. By inhibiting NO, EC-O2- production promotes T cell expansion during peripheral immune-response activation, not during tissue inflammation.Entities:
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Year: 2004 PMID： 15265676 DOI： 10.1016/j.jneuroim.2004.05.008
Source DB: PubMed Journal: J Neuroimmunol ISSN： 0165-5728 Impact factor: 3.478