REVIEW: Cytokines as Mediators of Neuroinflammation in Experimental Autoimmune Encephalomyelitis

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V. S. Gogoleva^1,2,a*, K.-S. N. Atretkhany^1,2, M. S. Drutskaya^1,2, I. A. Mufazalov³, A. A. Kruglov⁴, and S. A. Nedospasov^1,2,4,b*

¹Engelhardt Institute of Molecular Biology, Russian Academy of Sciences, 119991 Moscow, Russia

²Lomonosov Moscow State University, Biological Faculty, 119234 Moscow, Russia

³University of California, San Francisco, CA 94143, USA

⁴Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119234 Moscow, Russia

^* To whom correspondence should be addressed.

Received May 12, 2018; Revision received June 10, 2018

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Cytokines play a pivotal role in maintaining homeostasis of the immune system and in regulation of the immune response. Cytokine dysregulation is often associated with development of various pathological conditions, including autoimmunity. Recent studies have provided insights into the cytokine signaling pathways that are involved not only in pathogenesis of autoimmune neuroinflammatory disorders, such as multiple sclerosis, but also in neurodegenerative states, for example, Alzheimer’s disease. Understanding the exact molecular mechanisms of disease pathogenesis and evaluation of relevant experimental animal models are necessary for development of effective therapeutic approaches.

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KEY WORDS: experimental autoimmune encephalomyelitis, inflammation, neurodegeneration, proinflammatory cytokines, TNF, IL-6, IL-17A

DOI: 10.1134/S0006297918090110

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