info@biomedres.us   +1 (502) 904-2126   One Westbrook Corporate Center, Suite 300, Westchester, IL 60154, USA   Site Map
ISSN: 2574 -1241

Impact Factor : 0.548

  Submit Manuscript

OpinionOpen Access

Dual Role of Interleukin-37 As an Anti-Inflammatory and A Regulatory Cytokine In EAE

Volume 4 - Issue 1

Qi Xin, Lingyun Li, Zhong Huang and Zhangbo Chen*

  • Author Information Open or Close
    • Department of Pathogen Biology and Immunology, Shenzhen University School of Medicine, China

    *Corresponding author:Zhangbo Chen, Department of Pathogen Biology and Immunology, Shenzhen University School of Medicine, Nanhai Avenue 3688, Shenzhen 518060, Guangdong, China

Received: April 13, 2018;   Published: April 25, 2018

DOI: 10.26717/BJSTR.2018.04.000997

Full Text PDF

To view the Full Article   Peer-reviewed Article PDF

Abstract

Interleukin 37 (IL-37) was known as IL-1F7 before Nold and his colleagues renamed it. Nold believed that IL-37 which expressed on cells including macrophages or epithelial cells plays an anti-inflammatory effect under the condition of intracellular and extracellular. IL-37 almost completely suppresses the production of pro-inflammatory cytokines, whereas the abundance of these cytokines increased with silencing of endogenous IL-37 in human cells [1]. Most studies have now focused on the function of IL-37 as an anti-inflammatory cytokine, while other related functions are still being explored. An autoimmune disease is a condition in which the immune system attacks the body [2,3]. Recent research confirmed that IL-37 is associated with many autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), inflammatory bowel disease (IBD), and multiple sclerosis (MS) [4-7]. These studies have shown that IL-37 could inhibit proinflammatory cytokines such as TNF-α, IL-1α, IL-1β, IL-6, G-CSF and GM-CSF [1-3].

Abbreviations: SLE: Systemic Lupus Erythematosus; RA: Rheumatoid Arthritis; IBD: Inflammatory Bowel Disease; MS: Multiple Sclerosis; EAE: Experimental Allergic Encephalomyelitis; GM-CSF: Granulocyte Macrophage Colony Stimulating Factor

Opinion| Conclusion| References|