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T-Cell Subset Analysis of Lewis Lung Carcinoma Tumor Rejection: Heterogeneity of Effectors and Evidence for Negative Regulatory Lymphocytes Correlating with Metastasis

Division of Immunology and Rheumatology, Stanford University School of Medicine, Stanford, California 94305 [C. G.]; Baxter Healthcare Corporation, Santa Ana, California 92705 [R. S. G.]; and Department of Cell Biology, the Weizmann Institute, P.O. Box 76100, Rehovot, Israel [L. E., M. F.]

We have analyzed the phenotypes of the T-cell subsets generated in response to Lewis lung carcinoma clones in C57BL/6J recipients. The metastatic derivative, which expresses low levels of H-2K^b gene, predominantly elicited CD8, Vβ8, and Vβ9⁺ T-cells. The nonmetastatic clone expressing high levels of H-K^b gene triggered a more heterogeneous response of Vβ-5, -6, -8, -9, and -11 CD8⁺ T-cells. Comparison of the T-cell receptor (TCR) expression of the T-cells infiltrating the tumor site with the lymphocytes in the periphery of tumor-bearing animals revealed a pattern of homing of CD4⁺ T-cells bearing Vβ-5, -6, and -11 TCR chains and CD8⁺ T-cells bearing Vβ-5, -6, -9, and -11.

Depletion of Vβ5 or Vβ6⁺ T-cells correlated with accelerated tumor growth, implying their protective role as tumor-specific effectors and consistent with the cytotoxicity of T-cells with this TCR phenotype. Vβ11 TCR expression in the tumor-infiltrating lymphocytes increased with the tumor size. Depletion of Vβ11⁺ T-cells enhanced resistance to primary tumor growth and conferred protection from metastasis in recipients cleared of Vβ5 and Vβ6 T-cell subsets. Those results suggest that tumor-specific effectors as well as negative regulator T-cells home, infiltrate, and coexist in the tumor site.

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Received 5/29/92. Accepted 9/24/92.