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A Tumor-specific Th2 Clone Initiating Tumor Rejection via Primed CD8+ Cytotoxic T-Lymphocyte Activation in Mice

A Tumor-specific Th2 Clone Initiating Tumor Rejection via Primed CD8+ Cytotoxic T-Lymphocyte... We established a CD4 + T-cell clone specific for syngeneic methylcholanthrene-induced sarcoma, S1509a raised in an A/J mouse, involved in tumor regression. The phenotype of the T-cell clone was CD3 + , TCR-ß + , CD4 + , CD45RB + , LFA-1 + , ICAM-1 + , CD44 + , and VLA-4 + . The CD4 + T-cell clone specifically proliferated through antigen stimulation with attenuated S1509a in the presence of syngeneic accessory cells, and this antigen-induced proliferation was inhibited with anti-CD4 and anti-I-E k monoclonal antibodies. The CD4 + T-cell clone designated YS1093 secreted interleukin (IL) 4, IL-5, and IL-6, but not IFN- , tumor necrosis factor , or IL-2, thus indicating that the clone belongs to the Th2 type. YS1093 cells and their culture supernatant after antigen stimulation augmented the primed cytotoxic T lymphocyte killing activity at the effector phase. YS1093 cells having Th2-type characteristics made the homologous growing tumor regress in the tumor-bearing syngeneic mice when YS1093 cells were transferred into the tumor-bearing mice i.v. The in vivo tumor regression initiated by YS1093 cell transfer essentially required the presence of CD8 + T cells in the tumor-bearing hosts, thus suggesting that some specific Th2 cells are positively involved in tumor regression by activating primed CD8 + cytotoxic T lymphocytes against the homologous tumor in situ . 1 To whom requests for reprints should be addressed. Phone: (0888) 80-2317; Fax: (0888) 80-2320. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Cancer Research American Association of Cancer Research

A Tumor-specific Th2 Clone Initiating Tumor Rejection via Primed CD8+ Cytotoxic T-Lymphocyte Activation in Mice

Cancer Research , Volume 56 (21): 5005 – Nov 1, 1996

A Tumor-specific Th2 Clone Initiating Tumor Rejection via Primed CD8+ Cytotoxic T-Lymphocyte Activation in Mice

Cancer Research , Volume 56 (21): 5005 – Nov 1, 1996

Abstract

We established a CD4 + T-cell clone specific for syngeneic methylcholanthrene-induced sarcoma, S1509a raised in an A/J mouse, involved in tumor regression. The phenotype of the T-cell clone was CD3 + , TCR-ß + , CD4 + , CD45RB + , LFA-1 + , ICAM-1 + , CD44 + , and VLA-4 + . The CD4 + T-cell clone specifically proliferated through antigen stimulation with attenuated S1509a in the presence of syngeneic accessory cells, and this antigen-induced proliferation was inhibited with anti-CD4 and anti-I-E k monoclonal antibodies. The CD4 + T-cell clone designated YS1093 secreted interleukin (IL) 4, IL-5, and IL-6, but not IFN- , tumor necrosis factor , or IL-2, thus indicating that the clone belongs to the Th2 type. YS1093 cells and their culture supernatant after antigen stimulation augmented the primed cytotoxic T lymphocyte killing activity at the effector phase. YS1093 cells having Th2-type characteristics made the homologous growing tumor regress in the tumor-bearing syngeneic mice when YS1093 cells were transferred into the tumor-bearing mice i.v. The in vivo tumor regression initiated by YS1093 cell transfer essentially required the presence of CD8 + T cells in the tumor-bearing hosts, thus suggesting that some specific Th2 cells are positively involved in tumor regression by activating primed CD8 + cytotoxic T lymphocytes against the homologous tumor in situ . 1 To whom requests for reprints should be addressed. Phone: (0888) 80-2317; Fax: (0888) 80-2320.

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Publisher
American Association of Cancer Research
Copyright
Copyright © 1996 by the American Association for Cancer Research.
ISSN
0008-5472
Publisher site

Abstract

We established a CD4 + T-cell clone specific for syngeneic methylcholanthrene-induced sarcoma, S1509a raised in an A/J mouse, involved in tumor regression. The phenotype of the T-cell clone was CD3 + , TCR-ß + , CD4 + , CD45RB + , LFA-1 + , ICAM-1 + , CD44 + , and VLA-4 + . The CD4 + T-cell clone specifically proliferated through antigen stimulation with attenuated S1509a in the presence of syngeneic accessory cells, and this antigen-induced proliferation was inhibited with anti-CD4 and anti-I-E k monoclonal antibodies. The CD4 + T-cell clone designated YS1093 secreted interleukin (IL) 4, IL-5, and IL-6, but not IFN- , tumor necrosis factor , or IL-2, thus indicating that the clone belongs to the Th2 type. YS1093 cells and their culture supernatant after antigen stimulation augmented the primed cytotoxic T lymphocyte killing activity at the effector phase. YS1093 cells having Th2-type characteristics made the homologous growing tumor regress in the tumor-bearing syngeneic mice when YS1093 cells were transferred into the tumor-bearing mice i.v. The in vivo tumor regression initiated by YS1093 cell transfer essentially required the presence of CD8 + T cells in the tumor-bearing hosts, thus suggesting that some specific Th2 cells are positively involved in tumor regression by activating primed CD8 + cytotoxic T lymphocytes against the homologous tumor in situ . 1 To whom requests for reprints should be addressed. Phone: (0888) 80-2317; Fax: (0888) 80-2320.

Journal

Cancer ResearchAmerican Association of Cancer Research

Published: Nov 1, 1996

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