The regulatoy mechanism of IL-5-producing group 2 innate lymphoid cells by short-chain fatty acid

Research Project

Project/Area Number	16K19111
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Multi-year Fund
Research Field	Experimental pathology
Research Institution	Chiba University (2017) National Center for Global Health and Medicine (2016)
Principal Investigator	Kudo Fujimi 千葉大学, 大学院医学研究院, 特任助教 (30726419)
Project Period (FY)	2016-04-01 – 2018-03-31
Project Status	Completed (Fiscal Year 2017)
Budget Amount *help	¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000) Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000) Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Keywords	ILC2 / IL-5 / 喘息 / 炎症 / グループ2自然リンパ球 / 短鎖脂肪酸 / アレルギー / 免疫学
Outline of Final Research Achievements	Group 2 innate lymphoid cells (ILC2s) and type 2 helper T (Th2) cells produce Th2 cytokines including IL-5 and play important roles in asthma pathogenesis. Cyclosporin A (CsA) is a well-known immunosuppressant that is used against steroid-resistant asthma. We studied the effects of CsA in allergen-induced lung inflammation in mice and found that CsA decreased the number of lung ILC2s and attenuated papain-induced activation of ILC2s accompanied with IL-5 expression. The ILC2 suppression mediated by CsA was not observed in culture or in lymphocyte-deficient Rag2－/－ mice. Thus, we propose a new suppressive effect of CsA, i.e., administration of CsA indirectly suppresses maintenance and activation of lung ILC2s in addition to direct suppression of T cell activation and cytokine production.