| Project/Area Number |
17390106
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Human pathology
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| Research Institution | FUJITA HEALTH UNIVERSITY |
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Principal Investigator |
TSUTSUMI Yutaka FUJITA HEALTH UNIVERSITY, School of Medicine, Professor, 医学部, 教授 (80138643)
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| Co-Investigator(Kenkyū-buntansha) |
KAMOSHIDA Shingoa FUJITA HEALTH UNIVERSITY, School of Medicine, Senior assistant professor, 医学部, 講師 (70351020)
SHIMOMURA Ryoichi FUJITA HEALTH UNIVERSITY, School of Medicine, Assistant professor, 医学部, 助手 (20360232)
NAGASAKA Mitsuo FUJITA HEALTH UNIVERSITY, School of Medicine, Senior assistant professor, 医学部, 講師 (70410701)
KUROSAWA Yoshikazu FUJITA HEALTH UNIVERSITY, Institute for Comprehensive Medical Science, Professor, 総合医科学研究所, 教授 (10109259)
MIURA Keiji FUJITA HEALTH UNIVERSITY, Institute for Comprehensive Medical Science, Assistant professor, 総合医科学研究所, 助手 (20199946)
中野 浩 藤田保健衛生大学, 学長 (80097732)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥10,900,000 (Direct Cost: ¥10,900,000)
Fiscal Year 2006: ¥4,500,000 (Direct Cost: ¥4,500,000)
Fiscal Year 2005: ¥6,400,000 (Direct Cost: ¥6,400,000)
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| Keywords | inflammatory bowel disease / Crohn disease / ulcerative colitis / antibody-producing plasma cell / specific antigen / monoclonal antibody / 病変特異的抗体 / 病変局所 / クラーナリティ / 抗体mRNA / 酵素抗原法 / クローナリティ |
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| Research Abstract |
The purpose of our research is to find useful antibodies and antigens for analyzing the pathogenesis and for diagnosing and treating inflammatory bowel diseases (IBDs). In the lesions of IBDs, numbers of antibody-producing plasma cells infiltrate. However, the antigens recognized by antibodies produced in these immune cells remain unclear. Theoretically, the antibodies locally secreted within the lesions must be closely correlated with the disease process. We thus planned a research directly analyzing the antibodies produced by the plasma cells infiltrating in the lesion.
In the first year, we examined the clonality of cDNA encoding antibodies in mouse inflammatory colonic lesions experimentally provoked by dextran sodium sulfate administration, which represents a mouse model of ulcerative colitis. We identified clonalities of the antibody-producing cells infiltrating within the colonic lesion. Therefore, we assumed that the clonality of cDNA encoding antibodies might be useful as crite
… More
ria for identifying lesion-specific antibodies.
In the second year, we analyzed the clonality of antibody cDNA in regional lymph nodes obtained from horseradish peroxidase (HRP)-immunized rats. The HRP reactivity of single chain Fv (scFv) monoclonal antibodies synthesized from nodal tissue cDNA was pursued. We demonstrated clonalities in the nodal tissue cDNA encoding both the heavy and light chains. However, scFv monoclonal antibodies randomly synthesized from the cDNA lacked binding with HRP in the ELISA system. In order to identify cDNA encoding anti-HRP antibodies in the lymph nodes, we screened the cDNA library made from the immunized nodal tissue. Only one type of antibody clone was observed. By random sequence analysis, the heavy chain cDNA of this anti-HRP monoclonal antibody corresponded to one of the several clones. However, the light chain cDNA of the anti-HRP antibody was identical to the sequence that did not show any clonality. These results suggest to our regret that cDNA clones encoding antibody molecules do not necessarily indicate the lesion-specific antibodies. To overcome this difficulty, further analysis is now continuing. Less
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