1998 Fiscal Year Final Research Report Summary
Immunopathological defense mechanism by monocytoid B-lymphocytes and its role for the background of lymphomagenesis
| Project/Area Number |
09670182
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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 | Nagoya University |
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Principal Investigator |
ITO Masafumi School of Medicine, Nagoya University Associate Professor, 医学部, 助教授 (50184693)
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| Co-Investigator(Kenkyū-buntansha) |
FUJINO Masahiko School of Medicine, Assistant Professor, 医学部, 助手 (70262904)
NAKAGAWA Atsuko Aichi Medical University, Department of Pathology, Lecturer, 医学部, 講師 (90227736)
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| Project Period (FY) |
1997 – 1998
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| Keywords | splenic marginal zone / monocytoid B-cell / malignant lymphoma / LPS / MALTlymphoma / oncogenesis |
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| Research Abstract |
1. We investigated the experimental gastric ulcer of rat model by using immunohistochemistry. We observed B-lymphocytes infiltration around the small vessels in the ulcer lesions, and these lymphocytes rapidly differentiated into plasma cells at the same lesions.
2. By using prepared rat splenic marginal zone B-lymphocytes, we examined their differentiation under several cytokine addition. Their differentiation did not depend on the specific cytokine stimulation.
3. The separated rat marginal zone B-lymphocytes were labeled with non-specific FITC and injected intravenously. We followed these labeled lymphocytes by histology of the spleen. They were distributed in PALS and marginal zone at first and resided short time, and disappeared. We concluded that the splenic marginal zone was the zone of pooling and transit for monocytoid B-lymphocytes.
4. Histopathological examination of congenital and acquired immunodeficient patients, splenic marginal zone B-lymphocytes compensated the conventional B-cell deficiency. It speculated that marginal zone B-cells were activated compensated germinal center activation.
5. Malignant lymphoma cases of monocytoid B-cell subtype cases were examined clinicopathologically. Tissue localization and proceeding infection, such as Helicobacter infection of stomach, were important for oncogenesis.
6. Monocytoid B-cells induced by LPS had specific tissue affinity mediated by cell adhesion molecules as I-CAM.
7. Monocytoid B-cells activation in experimental rat. gastric ulcer were observed in ulcer lesion also splenic marginal zone. They showed the cell proliferating phase. We speculated they proliferated in each areas and moved through mucosa-marginal zone channel.
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