In vivo immunologic selection of class I major histocompatibility complex gene deletion variants from the B16-BL6 melanoma

J. E. Talmadge, C. B. Talmadge, B. Zbar, R. McEwen, A. K. Meeker, H. Tribble

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Abstract

The mechanism by which tumor allografts escape host immunologic attack was investigated. B16-BL6 cells (the bladder 6 subline of the B16 melanoma) (H-2b) were transfected with a gene (D(d)) encoding an allogeneic class I major histocompatibility complex antigen. Clones that expressed D(d) antigen were injected into the footpads of nonimmune syngeneic mice, syngeneic immune mice, and nude mice. Under conditions of immunologic selection a clone that contained multiple copies of the transfected gene formed variants that lacked the transfected gene. Primary tumors and pulmonary metastases of immunized mice and pulmonary metastases of nonimmunized mice had lost the D(d) gene and, in most cases, all of the associated plasmid. In contrast, in immunodeficient nude mice, primary tumors and pulmonary metastases retained the D(d) gene and the associated plasmid. Deletion of genes encoding cell surface antigens may be one of the mechanisms by which allogeneic tumors escape immunologic attack.

Original languageEnglish (US)
Pages (from-to)1215-1221
Number of pages7
JournalJournal of the National Cancer Institute
Volume78
Issue number6
StatePublished - Sep 25 1987

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ASJC Scopus subject areas

  • Oncology
  • Cancer Research

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