2021 Fiscal Year Final Research Report
Stress-induced renin causes intestinal inflammation via helper T cells
| Project/Area Number |
20K16280
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 49070:Immunology-related
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| Research Institution | Kyoto University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2022-03-31
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| Keywords | レニン / ヘルパーT細胞 / 炎症性腸疾患 |
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| Outline of Final Research Achievements |
Renin, which controls blood pressure, binds to (pro)renin receptor (PRR). Although hematopoietic cells express PRR, the function of PRR remain unclear. To address this question, we analyzed lymphocyte-specific PRR-deleted mice.
We found that T, B, and innate lymphoid cells were significantly reduced in PRR deficient mice. Furthermore, pro-renin enhanced helper T cell differentiation in vitro. Taken together, these results suggest a possibility that the signals of pro-renin receptor promote the development and maintenance of lymphocyte subsets to cause intestinal inflammation.
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| Free Research Field |
免疫学
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| Academic Significance and Societal Importance of the Research Achievements |
血圧を調整するレニンは細胞膜上の存在するプロレニン受容体に結合するが、受容体を発現する免疫細胞にどのような機能があるか、またシグナルを伝達し得るかこれまで不明であった。本研究から、レニンがアンジオテンシン経路を活性化するだけでなく、リンパ球の恒常性維持に寄与し、１型免疫応答や１７型免疫応答を制御することで、癌やウイルスの排除に効果を持つ一方で炎症性腸疾患の誘導に関わる可能性を見出した。これ結果から、血圧調整と免疫系が同時に制御される機構を発見することが期待され、高血圧と同時に起こり得る炎症性疾患発症の理解と治療に貢献する。
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