alexa IL-10 Modulates Th17 Pathogenicity during Autoimmune Di
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Review Article

IL-10 Modulates Th17 Pathogenicity during Autoimmune Diseases

Beichu Guo1,2*
1Department of Microbiology and Immunology, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425-5040, USA
2Hollings Cancer Center, Medical University of South Carolina (MUSC), Charleston, South Carolina 29425-5040, USA
*Corresponding Author : Beichu Guo, PhD
Department of Microbiology and Immunology
Hollings Cancer Center
Medical University of South Carolina (MUSC)
HO-612D, 86 Jonathan Lucas Street, Charleston
South Carolina 29425-5040, USA
Tel: 843-792-5708
E-mail: [email protected]
Received: January 29, 2015 Accepted: March 15, 2016 Published: March 22, 2016
Citation: Guo B (2016) IL-10 Modulates Th17 Pathogenicity during Autoimmune Diseases. J Clin Cell Immunol 7:400. doi: 10.4172/2155-9899.1000400
Copyright: © 2016 Guo B. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
 

Abstract

The immune system is essential for host defense against pathogen infections; however dysregulated immune response may lead to inflammatory or autoimmune diseases. Elevated activation of both innate immune cells and T cells such as Th17 cells are linked to many autoimmune diseases, including Multiple Sclerosis (MS), arthritis and inflammatory bowel disease (IBD). To keep immune homeostasis, the immune system develops a number of negative feedback mechanisms, such as the production of anti-inflammatory cytokine IL-10, to dampen excessive production of inflammatory cytokines and uncontrolled activation of immune cells. Our recent studies uncover a novel immunoregulatory function of interferon (IFN) pathways on the innate and antigen-specific immune response. Our results show that IFNα/β induced IL-10 production from macrophages and Th17 cells, which in turn negatively regulated Th17 function in autoimmune diseases such as Experimental Allergic Encephalomyelitis (EAE), an animal model of human MS. In a chronic colitis model resembling human IBD, we also found that IL-10 inhibited inflammasome/IL-1 pathway, and the pathogenicity of Th17 cells, leading to reduced chronic intestinal inflammation. Results from our and other studies further suggest that IL-10 produced by both macrophages and regulatory T cells may shift Th17 into more regulatory phenotypes, leading to reduced inflammatory response.

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