| Project/Area Number |
17390107
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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 | Kurume University |
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Principal Investigator |
OHSHIMA Koichi Kurume University, Pathology, Professor, 医学部, 教授 (50203766)
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| Co-Investigator(Kenkyū-buntansha) |
JIMI Shirou Fukuoka University, Pathology, Assistant Professor, 医学部, 助手 (30226360)
SUZUMIYA Junnji Fukuoka University, Pathology, Associate Professor, 医学部, 助教授 (70206556)
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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 |
¥8,000,000 (Direct Cost: ¥8,000,000)
Fiscal Year 2006: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥4,500,000 (Direct Cost: ¥4,500,000)
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| Keywords | T-cell lymphoma / HTLV-I / Lymph node / chemokine / chemokine receptor / ATLL / CCL18 / CX3CR1 |
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| Research Abstract |
Adult T-cell leukemia/lymphoma (ATLL) is a human malignancy associated with HTLV-I. The pathological features of the lymph nodes of ATLL change from those of lymphadenitis to Hodgkin-like features and those of lymphoma. Chemokines and their receptors are closely associated with T-cell subgroups and immune responses. To clarify the relationship between chemokines and their receptor expression, as well as the development of ATLL, 17 cases with ATLL were analyzed using DNA chips of chemokines and their receptors. All cases exhibited a varied and mixed pattern of up- and down- regulated gene expression of Th1, Th2, naive and cytotoxic cell-associated chemokine genes. Since CCL18 accounted for most up-regulated gene and CX3CR1 for most down-regulated gene, they were selected for immunohistochemical analysis. Immunohistochemical staining showed expression of the two genes in immunological cells, with a positive expression for reticulum cells, but not for ATLL cells. HTLV-I-associated lymphadenitis type (n=13) and Hodgkin-like type (n=12) cases showed significantly higher CCL18 expression than did non-specific lymphadenitis cases (n=10) (p<0.05). On the other hand, all HTLV-I associated cases showed significantly lower CX3CR1 expression than did non-specific lymphadenitis cases (p<0.05). These results suggest that up-regulation of CCL18 expression and down-regulation of CX3CR1 expression play a role in immune responses against the ATLL cells.
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