Functional analysis of an inhibitory receptor LMIR3 in basophil activation and Th2-type immune responses

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K19677
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Dermatology
• Research Institution: Juntendo University
• Principal Investigator: Izawa Kumi 順天堂大学, 医学(系)研究科(研究院), 助教 (80708313)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: 好塩基球 / ペア型レセプター / CD300

Outline of Final Research Achievements

Flow cytometric analysis showed that LMIR3 is not expressed in mouse tissue basophils, while it is highly expressed in mouse bone marrow-derived cultured basophils. LMIR3-deficient mice exhibited enhanced IgE-mediated chronic allergic inflammatory responses and IgG1/antigen-dependent passive systemic anaphylactic responses than did wild-type counterparts. This might be because inflammatory tissue basophils express LMIR3, inhibiting IgE- or IgG-dependent activation of basophils or because these responses are suppressed by LMIR3 in immune cells other than basophils. On the other hand, LMIR3-deficient basophils or dendritic cells highly induced Th2 responses as compared with wild-type counterparts, indicating that LMIR3 inhibits Th2-mediated allergic responses.

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