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Selective inhibition of human glial inducible nitric oxide synthase by interferon‐β: Implications for multiple sclerosis
Author(s) -
Hua Liwei L.,
Liu Judy S. H.,
Brosnan Celia F.,
Lee Sunhee C.
Publication year - 1998
Publication title -
annals of neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.764
H-Index - 296
eISSN - 1531-8249
pISSN - 0364-5134
DOI - 10.1002/ana.410430317
Subject(s) - nitric oxide synthase , multiple sclerosis , nitric oxide , interferon gamma , interferon , pathogenesis , microglia , immunology , central nervous system , inflammation , biology , chemistry , cytokine , neuroscience , endocrinology
Nitric oxide generated from the inducible nitric oxide synthase (iNOS) has been implicated in the pathogenesis of multiple sclerosis. Because significant species‐ and cell‐specific differences exist in the expression of iNOS, we used primary human glial cell cultures to screen for an inhibitor of iNOS expression. Remarkably, among numerous soluble factors tested, interferon‐β (IFN‐β) alone showed a selective and potent inhibition of interleukin‐1β/interferon‐γ (IL‐1β/IFN‐)–induced iNOS expression in astrocytes. Inhibition of iNOS may provide a mechanism by which IFN‐β can ameliorate inflammation and cytotoxicity in the central nervous system of patients with multiple sclerosis.