| Project/Area Number |
11670169
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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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 | Tokyo Medical and Dental University |
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Principal Investigator |
TANIZAWA Toru Tokyo Medical and Dental University, Graduate School of Allied Health Sciences, Instructor, 大学院・保健衛生学研究科, 助手 (00227232)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 2001: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2000: ¥600,000 (Direct Cost: ¥600,000)
Fiscal Year 1999: ¥900,000 (Direct Cost: ¥900,000)
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| Keywords | malignant lymphoma of stomach / Helicobacter pylori / lymphoid hyperplasia / chronic gastritis / follicular gastritis / リンパ組織過形成 / 異悪性リンパ腫 / リンパ濾胞過形成 |
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| Research Abstract |
1. Histopathological examinations ;
(1) Lymphoid follicle hyperplasia in the gastirc mucosa and its structure : Lymphoid follicle hyperplasia in the gastric mucosa was chiefly caused by Helicobacter-pylori infection. An aggregation of CD4-positive T cells was thought to be an important component of the lymphoid follicle.
(2) Proliferate activity of B cells and T cells in the lymphoid tissue of gastric mucosa : Proliferative activity of B cells out of germinal center was significantly accelerated in gastric malignant lymphoma cases. Follicular gastritis cases exhibited an intermediate value between lymphoma cases and active gastritis cases without lymphoid hyperplasia. There was no correlation between lymphoid follicle hyperplsia and proliferative activity of B cells. Proliferative activity of T cells was significantly accelerated in follicular gastritis cases, and exhibited positive correlation to the score of secondary lymphid follicles.
(3) Difference of the pathogenesis between follicular gastritis and gastric malignant lymphoma : Follicular gastritis was caused by activation of T cells by Helicobacter-pylori infection, and did not necessarily result in abnormal acceleration of B-cell proliferation.
2. Study of immunoglobulin heavy-chain gene rearrangement by PCR method ; In the present study clonal proliferation of B cells was not demonstrated in gastritis cases. It was owing to the more decreased sensitivity of the system (materials) used in this study than the reported system.
3. Lymphoid follicle hyperplasia did not necessarily reflect the accelerated proliferative activity of B cells, and follicular gastritis had no direct relation to the generation of malignant lymphoma. In the future the search for factors which reflect the accelerated proliferative activity of B cells is required.
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