| Project/Area Number |
05670211
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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 |
Experimental pathology
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| Research Institution | The JIKEI University School of Medicine |
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Principal Investigator |
JOH Kensuke JIKEI University School of Medicine, Associate Professor, 医学部, 助教授 (10057086)
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| Co-Investigator(Kenkyū-buntansha) |
OHKAWA Kiyoshi JIKEI University School of Medicine, Professor, 医学部, 教授 (90112812)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1994: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1993: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | Hapten / Trinitrophenol / Renal tubular basement membrane / Organ allergy / Cationic protein / Ovalbumin / Cellular immunity / Interstitial nephritis / trinitrophenol / 卵白アルブミン |
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| Research Abstract |
Trinitrophenol-conjugated ovalbumin was highly cationized (isoelectric point>10) and was subjected to gel filtration to obtain monomer (42 kDa). The antigen was injected selectively into the left renal arteries of Wistar rats. Antigen localization was documented by immunohistochemistry on frozen section ; it was deposited in a liner pattern on the tubular basement membrane (TBM) and Bowman's capsule but not on the glomerular basement membrane, and remained up to 36 h after the antigen injection. In control, non-cationized, monomeric TNP-OA (42 kDa, isoelectric point=4.6) showed fine granular deposition in the tubular epithelium exclusivery, but not on the TBM.Tubulointerstitial nephritis (TIN) with neutrophilic infiltration was induced by the serum transfer of antiTNP-human IgG rabbit serum 24 h after cationic antigen injection. Acute tubular necrosis was induced after cationic antigen injection in the rats which were 7 days-previously skin-sensitized by picryl chloride to have TNP-specific cellular immunity. The lesion was not similar to the lesion of human hypersensitivity nephritis and may due to the TNP-toxicity. The transfer of splenic T cell (either CD4+ or CD8+) against TNP did not contribute to TIN-induction in the non-sensitized C57/BL6 mice which were previously injected with the cationic antigen.
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