2020 Fiscal Year Final Research Report
Functional analysis of Semaphorin against differentiation control of monocyte subsets and impaired macrophage clearance.
Project/Area Number |
19K17840
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 54010:Hematology and medical oncology-related
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Research Institution | Kagawa Prefectural College of Health Sciences |
Principal Investigator |
Yamaguchi Wataru 香川県立保健医療大学, 保健医療学部, 助教 (70611713)
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Project Period (FY) |
2019-04-01 – 2021-03-31
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Keywords | 鉄代謝 / 赤脾髄マクロファージ / セマフォリン / 免疫不全 |
Outline of Final Research Achievements |
Iron has been reported to accumulate in the spleen tissue of many immunodeficient mice. Particularly, splenic iron accumulation was observed in immunodeficient Sema4D-deficient mice , and its cause was aimed to be elucidated in this study. Iron that accumulates in the spleen is derived from erythrocytes , wherein waste erythrocytes are phagocytosed and stored by splenic red pulp macrophages. We showed that the phagocytic capacity of the red pulp macrophages was enhanced and the number of the cells was increased in Sema4D-deficient mice. These suggest that the increase in red pulp macrophages increased the splenic iron accumulation.
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Free Research Field |
血液・腫瘍内科学
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Academic Significance and Societal Importance of the Research Achievements |
免疫不全は重篤な感染症を繰り返し引き起こし、また鉄の代謝異常は貧血や鉄過剰症に繋がることがあり、その関連について研究することは非常に重要である。これまでは感染症に伴うヘプシジンホルモンの影響により鉄が蓄積すると考えられていた。しかし本研究では免疫不全を呈するマウスにおいて、赤脾髄マクロファージの増加を認め、その鉄代謝バランスの異常により脾臓に鉄が蓄積することを明らかにし、新たな鉄蓄積のメカニズムを報告した。
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