2015 Fiscal Year Final Research Report
Role of DOCK2 in antigen-specific humoral immunity
Project/Area Number |
24590586
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Research Category |
Grant-in-Aid for Scientific Research (C)
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Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Immunology
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Research Institution | Kitasato University (2013-2015) Kyushu University (2012) |
Principal Investigator |
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Project Period (FY) |
2012-04-01 – 2016-03-31
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Keywords | B細胞 / 抗原応答 / シグナル伝達 / 抗体産生 |
Outline of Final Research Achievements |
The small G protein Rac is known to play important roles in B cell activation by acting downstream of B cell receptor (BCR). We found that DOCK2, an atypical Rac activator predominantly expressed in hematopoietic cells, is essential for BCR-mediated Rac activation.DOCK2-deficient B cells failed to form immunological synapse and displayed impaired antigen-stimulated growth in vitro. DOCK2 knock-out mice were shown to have impaired production of antibody in response to antigen immunization, indicating DOCK2 plays a critical role in humoral immunity.
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Free Research Field |
免疫学
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