2004 Fiscal Year Final Research Report Summary
Regulation of integrin-mediated adhesion and immune response by Rap1 and its downstream effector, p30.
| Project/Area Number |
15590436
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Immunology
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| Research Institution | Kyoto University |
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Principal Investigator |
KATAGIRI Koko Kyoto University, Graduate School of Medicine, lecturer, 医学研究科, 講師 (00322157)
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| Co-Investigator(Kenkyū-buntansha) |
KINASHI Tatsuo Kyoto University, Graduate School of Medicine, professor, 医学研究科, 教授 (30202039)
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| Project Period (FY) |
2003 – 2004
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| Keywords | Rap1 / RAPL / Integrin / cell polarization / migration / homing / chemokine / adhesion |
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| Research Abstract |
Immunosurveillance requires the coordinated regulation of chemokines and adhesion molecules to guide immune cell migration. However, the critical molecule to govern high trafficking capability of immune cells is not clear. We showed that RAPL plays indispensable roles in integrin-mediated adhesion and migration of lymphocytes and dendritic cells. RAPL deficiency causes defective chemokine-triggered lymphocyte adhesion and migration to secondary lymphoid organs, resulting in atrophic lymphoid follicles and deficient marginal zone B cells, concomitant with increased immature B cells in the blood. Furthermore, splenic dendritic cells were diminished and defective in adhesion. Upon activation with inflammatory stimuli, skin and splenic dendritic cells failed to migrate into either the draining lymph nodes or the white pulp of the spleen. Thus, RAPL is a crucial immune cell trafficking regulator essential for immunosurveillance.
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