| Co-Investigator(Kenkyū-buntansha) |
INABA Takashi Hirosaki University School of Medicine, Department of Parasitology, Associated Professor, 医学部, 助教授 (60003612)
KAMIYA Haruo Hirosaki University School of Medicine, Department of Parasitology, Professor, 医学部, 教授 (70002079)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2002: ¥1,800,000 (Direct Cost: ¥1,800,000)
Fiscal Year 2001: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
To assess the potential role of IgA antibody in expulsion of the nematode from the intestine, a panel of IgA monoclonal antibodies (mAbs) were produced from the mesenteric lymph nodes of BALB/c mice orally vaccinated with irradiated muscle larvae of Trichinella britovi. One IgA mAb, HUSM-Tb1, formed immunoprecipitates on the surface of live muscle larvae, and by immunohistochemistry reacted with their stichocytes and cuticular surface. Intraperitoneal injection of BALB/c mice with this mAb 5 hours before challenge conferred a high level of protection (more than 95%) against Trichinella infection, when 2.0 mg of specific IgA per 20 g body weight was given to a mouse. The same treatment produced a similar effect in SCID mice and rats, but not in Mongolian jirds (Meriones unguiculatus). In vivo clearance of intraperitoneally-injected IgA mAb was different between mice and jirds. In mice, more than a half of detectable fecal IgA was excreted within 5 hours after injection, and the excretio
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n was almost completed within 12 hours. In contrast, jirds excreted more then a half of detectable fecal IgA between 5 and 12 hours after injection, and completed its excretion by 24 hours. Correlating with it, prolonged retention of more IgA in the blood was noticed in jirds than mice. It is speculated that jirds might have some defect(s) in mucosal transportation of murine IgA, and it is needed to explore more on the mucosal IgA defense system unique to jirds.
Along with the works mentioned above, we have performed the following observations to clarify the characteristics of jird immune systems; 1) complement activity using the complement-dependent anti-Thy-1 glomerulonephritis model, 2) T-cell dependent elimination of intestinal cestode (Taenia crassiceps) infection and blood trypanosome (Trypanosoma grosi) infection, by use of T-cell-depleted jirds using anti-jird T-cell mAb (HUSM-M.g.15), 3) In vivo interaction of jird cutaneous dendritic cells with skin-penetrating parasites (Schistosoma mansoni) by use of anti-jird MHC class II mAb (HUSM-M.g.30), and 4) characterization of two IgG subclasses in jirds and temporal changes in humoral immune responses of T-cell-depleted, T. grosi-infected jirds. These works increase our knowledge on the unique immune defense system of Mongolian jirds that are highly useful as a laboratory model of various infectious diseases of medical importance. Less
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