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Critical Reviews™ in Immunology
Facteur d'impact: 1.352 Facteur d'impact sur 5 ans: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN Imprimer: 1040-8401
ISSN En ligne: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.v21.i5.20
23 pages

lnterleukin-10 in the Brain

Klemen Strle
Laboratory of Immunophysiology , Department of Animal Sciences , College of Medicine, University of Illinois, Urbana, IL 61801
Jian-Hua Zhou
Laboratory of Immunophysiology , Department of Animal Sciences, University of Illinois, Urbana, IL 61801
Wen-Hong Shen
Laboratory of Immunophysiology, Department of Animal Sciences, University of Illinois, Urbana, IL 61801
Suzanne R. Broussard
Laboratory of Immunophysiology, Department of Animal Sciences, University of Illinois, Urbana, IL 61801
Rodney W. Johnson
lntegrative Biology, Department of Animal Sciences, University of Illinois, Urbana, IL 61801
Gregory G. Freund
Department of Pathology, College of Medicine, University of Illinois, Urbana, IL 61801
Robert Dantzer
INRA-INSERM U394, Unite de Recherches de Neurobiologie Integrative, Institute Francois Magendie, Rue Camille Saint-Saens, 33077 Bordeaux, France
Keith W. Kelley
Laboratory of Immunophysiology, Department of Animal Sciences, University of Illinois, Urbana, IL 61801

RÉSUMÉ

Interleukin (IL)-10 is synthesized in the central nervous system (CNS) and acts to limit clinical symptoms of stroke, multiple sclerosis, Alzheimer's disease, meningitis, and the behavioral changes that occur during bacterial infections. Expression of IL-10 is elevated during the course of most major diseases in the CNS and promotes survival of neurons and all glial cells in the brain by blocking the effects of proapoptotic cytokines and by promoting expression of cell survival signals. Stimulation of IL-10 receptors regulates numerous life- or death-signaling pathways—including Jakl/Stat3, PI 3-kinase, МАРК, SOCS, and NF-kВ—ultimately promoting cell survival by inhibiting both ligand- and mitochondrial-induced apoptotic pathways. IL-10 also limits inflammation in the brain; it does so by three major pathways: (1) reducing synthesis ofproinflammatory cytokines, (2) suppressing cytokine receptor expression, and (3) inhibiting receptor activation. Finally, IL-10 induces anergy in brain-infiltrating Т cells by inhibiting cell signaling through the costimulatory CD28-CD80/86 pathway. The multiple functions of IL-10 in the brain will create new and intriguing vistas that will promote a better understanding of neurodegenerative diseases. These discoveries could lead to development of innovative approaches for the use of anti-inflammatory cytokines in major debilitating diseases of the CNS.


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