| Project/Area Number |
01570427
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Respiratory organ internal medicine
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| Research Institution | Second Division, Department of Internal Medicine, Hamamatsu University School of Medicine. |
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Principal Investigator |
CHIDA Kingo Hamamatsu University School of Medicine, Assistant Professor, 医学部, 助手 (40197611)
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| Co-Investigator(Kenkyū-buntansha) |
SATO Atsuhiko Hamamatsu Univertity School of Medicine, Associate Professor, 医学部, 助教授 (60027109)
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| Project Period (FY) |
1989 – 1990
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| Project Status |
Completed (Fiscal Year 1990)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1990: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1989: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | Alveolar Macrophage / Activated Macrophage / Anti Rabbit Antibody / Function Associated Antigen / Monoclonal Antibody / Phagocytosis / BCG / 抗肺胞マクロファ-ジ単クロ-ン性抗体 / 家兎肺胞マクロファ-ジ / 表面膜抗原 |
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| Research Abstract |
We produced a monoclonal antibody against rabbit activated alveolar macrophage, in order to clarify the immunological roles of lung macrophages. BALB/c mice were immunized with bronchoalveolar lavage (BAL) cells obtained from a rabbit sensitized by heat-killed BCG intravenous injection. Spleen cells prepared from these mice were fused with the NS-1 plasmacytoma cell line using hybridoma technology, and we raised a monoclonal antibody called AM-1. The screening and characterization of this monoclonal antibody were carried out employing cellular radioimmunoassay, flow cytometric analysis, and immunohistochemical methods. AM-1 did not react with either blood monocytes or BAL-macrophages obtained from normal rabbits, but was positive for BAL-macrophages from BCG vaccinated rabbits. The percentage of positive cells for BAL-macrophages from rabbits at 7 days after vaccination was about 90%. The positive rate gradually decreased in relation to the time since BCG sensitization. The immunoglobulin subclass of AM-1 was IgG2b checked by Ouchterlony's method. Interestingly, incubation with either 10% fetal calf serum or macrophage activating factor caused increases in AM-1 reactivity of alveolar macrophages, and pretreatment of alveolar macrophages with AM-1 resulted in significantly reduced phagocytic capacity.
These results indicates that expression of surface anti AM-1 antigen is associated with an early activation process of alveolar macrophages, and also suggests that expression of anti AM-1 antigen appears to be involved in some of the macrophage functions.
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