A novel regulatory mechanism of C-type lectin receptor-mediated antifungal immunity

2019 Fiscal Year Final Research Report

• Project/Area Number: 18K15195
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 49070:Immunology-related
• Research Institution: Osaka University
• Principal Investigator: Toyonaga Kenji 大阪大学, 微生物病研究所, 特任研究員(常勤) (90791567)
• Project Period (FY): 2018-04-01 – 2020-03-31
• Keywords: 自然免疫受容体 / 真菌感染症

Outline of Final Research Achievements

Candida albicans (C. albicans), which colonize the skin and mucous membranes as a resident fungus, causes severe symptoms such as disseminated candidiasis as an opportunistic infection. For the protection against C. albicans, activation of innate immunity through the C-type lectin receptors (CLRs) such as Dectin-1/Dectin-2 and its signaling adaptor molecule CARD9 plays an important role. However, the detailed regulatory mechanism of this pathway is still unknown. In this study, we found that Trem2 (triggering receptor expressed on myeloid cells 2) might contribute to the suppression of CLR-mediated activation signals.

Free Research Field

感染免疫学

Academic Significance and Societal Importance of the Research Achievements

全身性カンジダ症のマウスモデルを用いた報告や、様々な疫学的知見から、C. albicansに対する感染防御には、Dectin-1/Dectin-2-CARD9経路を介した自然免疫応答の活性化が重要であることが明らかとなっている。この経路を抑制することが知られているCbl-bの阻害剤は、C. albicansの排除応答を促進することも報告されているため、Trem2-Dap12経路の阻害がカンジダ症の新規治療につながる可能性がある。