| Project/Area Number |
03670348
|
|---|
| Research Category |
Grant-in-Aid for General Scientific Research (C)
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Gastroenterology
|
|---|
| Research Institution | University of Tsukuba. |
|---|
Principal Investigator |
KOYAMA Shohei Dept. Int. Med. Assistant Prof. Univ. of Tsukuba, 臨床医学系, 講師 (00110502)
|
|---|
| Co-Investigator(Kenkyū-buntansha) |
FUKAO Katashi Dept. Surg. Prof. Univ. of Tsukuba., 臨床医学系, 教授 (50091921)
|
|---|
| Project Period (FY) |
1991 – 1992
|
| Project Status |
Completed (Fiscal Year 1992)
|
| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1991: ¥1,400,000 (Direct Cost: ¥1,400,000)
|
|---|
| Keywords | gastric carcinoma / killer T cells (CTL) / suppressor cells / ICAM-1 / Adhesion molecules / LAK cells / TIL / キラ-T細胞 / サプレッサ-T細胞 / ICAMー1 / LFAー1 |
|---|
| 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.
|
