Definition of a unique cell surface antigen of mouse leukemia RL♂1 by cell-mediated cytotoxicity Academic Article Article uri icon

Overview

MeSH Major

  • Antigens, Neoplasm
  • Genetic Therapy
  • HLA-A2 Antigen
  • Immunologic Factors
  • Immunotherapy, Active
  • Interleukin-2
  • Melanoma
  • Recombinant Fusion Proteins
  • Tumor Cells, Cultured

abstract

  • BALB/c x-ray-induced leukemia RL male 1 is strongly immunogenic for (BALB/c x C57BL/6)F1 mice. Transplants of RL male 1 regressed after initial growth, and after tumor regression mice could resist repeated inocula of 10(7) RL male 1 cells. Spleen cells from immunized mice after in vitro stimulation with RL male 1 were cytotoxic for RL male 1 cells in 3-hr 51Cr assays. Pretreatment of immune spleen cells with Thy-1, Lyt-2, or Lyt-3 antisera and complement eliminated cytotoxic activity, indicating that effector cells for RL male 1 lysis are T cells. Tests with other target cells showed little or no cytotoxicity. Analysis of the specificity of T-cell killing of RL male 1 by competitive inhibition assays with unlabeled cells indicated that only RL male 1 could inhibit killing; other BALB/c tumors (13 x-ray or murine leukemia virus-induced leukemias and three myelomas) failed to inhibit lysis of RL male 1. A range of alloantisera and heteroantisera were tested for their capacity to block lytic activity in the absence of added complement. H-2d antisera and Lyt-2 and -3 antisera blocked lysis, the latter at the level of the effector cell. Antisera to other cell surface alloantigens, murine leukemia virus-related antigens, and immunoglobulins did not block RL male 1 lysis. Thus, T cells from mice immunized against RL male 1 recognize an individually distinct or unique antigen that does not appear to be related to any of the serologically defined cell surface determinants of RL male 1. In its restriction to a single leukemia, the RL male 1 antigen resembles the individually distinct antigens of chemically induced tumors and other tumor types of rodents.

publication date

  • December 1979

Research

keywords

  • Academic Article

Identity

Digital Object Identifier (DOI)

  • 10.1073/pnas.76.7.3486

PubMed ID

  • 91166

Additional Document Info

start page

  • 3486

end page

  • 90

volume

  • 76

number

  • 7