The elucidation of novel mechanisms for regulation of allergic inflammation by serotonin

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K16702
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 49070:Immunology-related
• Research Institution: Institute of Physical and Chemical Research
• Principal Investigator: Kiniwa Tsuyoshi 国立研究開発法人理化学研究所, 生命医科学研究センター, 基礎科学特別研究員 (90793795)
• Project Period (FY): 2019-04-01 – 2021-03-31
• Keywords: アレルギー / 気管支喘息 / ILC2 / セロトニン / マスト細胞

Outline of Final Research Achievements

Group 2 innate lymphoid cells (ILC2) are important lymphocytes in the pathogenesis of allergy same as type 2 helper T cells (Th2 cells). In this study, we analyzed the mechanism of serotonin-induced suppression of ILC2 using a mouse model of bronchial asthma. Serotonin treatment suppressed ILC2 function in the asthmatic lungs and markedly reduced allergic inflammation. RNAseq analysis revealed that serotonin selectively suppressed activated ILC2, but not naive ILC2 or Th2 cells. Furthermore, we demonstrated that the serotonin source of asthmatic lungs was mast cells in the bronchial epithelial layer, suggesting that they play a role in preventing excessive activation of ILC2.

Free Research Field

自然免疫学

Academic Significance and Societal Importance of the Research Achievements

本研究によって、非常に多機能な生理活性モノアミンであるセロトニンが、アレルギー性疾患の新たな治療標的として注目を集めているILC2に対して選択的な抑制作用を持つことが明らかとなった。セロトニン拮抗薬はうつ病、偏頭痛など様々な疾患を対象に薬として使われており、本研究の成果をもとに、今後アレルギー治療に応用されることが期待される。