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Research Article Free access | 10.1172/JCI118946

Soluble tumor necrosis factor receptor inhibits interleukin 12 production by stimulated human adult microglial cells in vitro.

B Becher, V Dodelet, V Fedorowicz, and J P Antel

Montréal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Canada.

Find articles by Becher, B. in: JCI | PubMed | Google Scholar

Montréal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Canada.

Find articles by Dodelet, V. in: JCI | PubMed | Google Scholar

Montréal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Canada.

Find articles by Fedorowicz, V. in: JCI | PubMed | Google Scholar

Montréal Neurological Institute, Department of Neurology and Neurosurgery, McGill University, Canada.

Find articles by Antel, J. in: JCI | PubMed | Google Scholar

Published October 1, 1996 - More info

Published in Volume 98, Issue 7 on October 1, 1996
J Clin Invest. 1996;98(7):1539–1543. https://doi.org/10.1172/JCI118946.
© 1996 The American Society for Clinical Investigation
Published October 1, 1996 - Version history
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Abstract

IL-12 is a cytokine detected in active lesions in multiple sclerosis (MS) and promotes the acquisition of a Th1 cytokine profile by CD4+ T cells. Autoreactive T cells recovered from the central nervous system of animals with experimental autoimmune encephalomyelitis (EAE), a disease model for MS, display this phenotype. We demonstrate that human central nervous system-derived microglia, but not astroglia, can produce IL-12 in vitro. Under basal culture conditions, human adult microglia do not express detectable levels of IL-12, although these cells show some degree of activation as assessed by expression of the immunoregulatory surface molecules HLA-DR and B7 as well as low levels of TNF-alpha mRNA. Following activation with LPS, IL-12 p40 mRNA and p70 protein can be readily detected. IL-12 production is preceded by TNF-alpha production and is inhibited by recombinant soluble human TNF receptor (II)-IgG1 fusion protein (shu-TNF-R). These data indicate regulation of IL-12 by an autocrine-dependent feedback loop, providing an additional mechanism whereby shu-TNF-R, now used in clinical trials in MS, may be exerting its effect.

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