2007 Off Campus Research Internship Awardee

Jasmine Shafagh (Biology)


Functional Interleukin-17 Receptor A is Expressed in the Central Nervous System and Upregulated in Experimental Autoimmune Encephalomyelitisa

Jayasri Das Sarma1, Bogoljub Ciric1, Ryan Marek1, Sanjoy Sadhukhan1, Jasmine Shafagh1, Denise C. Fitzgerald1, Kenneth S. Shindler2 and A. M. Rostami1*
1Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107.
2Department of Ophthalmology, University of Pennsylvania, Scheie Eye Institute and FM Kirby Center for Molecular Ophthalmology, Philadelphia, PA 19104.


Running title: Expression and signaling of IL-17RA in the CNS


Interleukin-17A (IL-17A) is founding member of a novel family of inflammatory cytokines that plays a critical role in the pathogenesis of many autoimmune diseases, including multiple sclerosis (MS) and its animal model, experimental autoimmune encephalomyelitis (EAE). IL-17A signals through IL-17RA, which is expressed in most peripheral tissues; however, expression of IL-17RA in the central nervous system (CNS) and its role in CNS inflammation are not well understood. Here we report constitutive expression of functional IL-17RA in mouse CNS tissue. Specifically, CNS astrocytes and microglia express IL-17RA, and IL-17A treatment induces biological responses in these cells in vitro. In response to exogenous IL-17A treatment, microglia and astrocytes significantly upregulate MCP-1, MCP-5, MIP-2 and KC chemokine secretion. Exogenous IL-17A does not significantly alter the constitutive expression of IL-17RA mRNA in glial cells, suggesting that upregulation of chemokines by glial cells is due to IL-17A signaling through constitutively expressed IL-17RA. IL-17RA expression is significantly increased in the CNS of mice with EAE compared to healthy mice. Our findings suggest that IL-17RA signaling in glial cells can play a significant role in autoimmune inflammation of the CNS and may be a potential pathway to target for therapeutic interventions.

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