1992 Fiscal Year Final Research Report Summary
Molecular mechanisms of Tumor-cytolysis by CTL against gastric carcinoma.
| Project/Area Number |
03670348
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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 |
Gastroenterology
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| Research Institution | University of Tsukuba. |
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Principal Investigator |
KOYAMA Shohei Dept. Int. Med. Assistant Prof. Univ. of Tsukuba, 臨床医学系, 講師 (00110502)
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| Co-Investigator(Kenkyū-buntansha) |
FUKAO Katashi Dept. Surg. Prof. Univ. of Tsukuba., 臨床医学系, 教授 (50091921)
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| Project Period (FY) |
1991 – 1992
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| Keywords | gastric carcinoma / killer T cells (CTL) / suppressor cells / ICAM-1 / Adhesion molecules / LAK cells / TIL |
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| Research Abstract |
1) Malignant pleural or peritoneal effusion-associated lymphoid (EAL) cells from patients with advanced carcinoma were cultured with autologous carcinoma with autologous carcinoma cells in the presence of rIL-2 or T-cell growth factor (TCGF: culture supernatant of PHA-stimulated spleen cells). Consequently, the majority of killer-effector cells against allogeneic cells in rIL-2-activated EAL cells from cancer patients showed CD4^+Leu8^-phenotype. In contrast, the cytolytic activity against autologous or allogeneic tumor cells in TCGF-activated EAL cells was mediated by CD8^+CD11b^- and CD8^+CD28^+ effector cells.
2) The CTL activity was mediated by CD2, CD3/TCR complex, CD8 and ICAM-1 molecules. However, LAK activity was mediated by CD2, CD4 and ICAM-1, but not by CD3/TCR, and HLA-Class 1 antigen.
3) TCGG-activated suppressor (LAS) effector cell populations responsible for suppression of cell-mediated antitumor immunity reside within CD8^+CD11b^- T cells.
4) Circulating suppressor cells with surface phenotype of CD8^+ or possible CD8^-CD11b^+ from freshly prepared PBL in patients with advanced gastric carcinoma are noted. The suppression of immunity was clearly directed at the effector process performed by CTL or LAK cells.
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