Mechanism of Th17 and Treg in Allergic Rhinitis

¹ The High School Affiliated to Renmin University of China, Beijing, 100000, China
² Department of Immunology, Institute of Basic Medical Sciences, Chinese Academy of Medical Sciences; School of Basic Medicine, Peking Union Medical College, Beijing 100730, China

^* Corresponding author’s: e-mail: Linda13311207892@outlook.com

Abstract

Allergic rhinitis (AR) influenced over half billion people around the globe, and its mechanism had been studied for long. While the role of Th1 and Th2 in AR was supported by substantial evidence, the relationship between Th17, Tregs, and AR was less researched. The role of Th17 and Tregs was less understood and sometimes downplayed. However, Recent studies suggested a close relationship between Th17, Tregs, and AR. Th17 and Treg secreted cytokines that could promote or attenuate inflammation and other AR symptoms via interaction with other molecules, cells, and pathways. This essay summarized these studies, and might provide a more thorough insight on AR mechanism and potential AR treatments. Th17 enhanced AR through the release of proinflammatory cytokines, including IL-17 that induced other immune cell response through multiple pathways, increased IgE production via interaction with other interleukins and cells, and promoted the release of other pro-inflammatory mediators. Tregs inhibited inflammation of via the release of anti-inflammatory cytokines including IL-10 and TGF-β, which suppressed the response of other immune cells such as T cell, B cell, eosinophil, and mast cell, inhibited IgE function via regulated immune cell response, and decreased pro-inflammatory factor release through involvement in the STAT3 related pathway. Based on these studies, several potential AR treatments emerged, as anti-IL-17-neutralizing antibodies, anti-IL-33 antibodies, and CC10 effectively inhibited inflammation, and probiotic NVP-1703 reduced rhinorrhea, nasal congestion, watery eyes, and sleep disturbance, though further research was necessary in order to comprehensively examine and compare the efficacy of these treatments. Understanding the role of Th17 and Treg could help researchers develop new drug that target specific messenger in signalling transduction pathways of Th17 and Treg cytokines that might augment or attenuate AR symptoms or immune response, giving rise to a probability of AR treatments with less adverse effects and stronger efficacy in the future.