In vivo or in vitro immunity to murine leukemia virus (MuLV)-induced leukemia cells which do not effectively produce virus, has been difficult to demonstrate. Because immunizations with allogeneic murine leukemia cells have been used to confer syngeneic tumor immunity to virus- producing cells, we attempted to generate lymphocytes, cytotoxic to syngeneic nonproducer leukemia cells, by stimulating normal murine spleen cells with allogeneic nonproducer leukemia cells in mixed tumor lymphocyte culture (MTLC) reactions in vitro. Secondary allogeneic MTLC of normal C57BL/6 or DBA/2 spleen cells effectively produced syngeneic tumor-specific cytotoxic lymphocytes. Target cells lysed in lymphocyte- mediated cytolysis (LMC) assays, included both Friend and Rauscher virus- induced syngeneic murine leukemia cells and chemically-induced hematopoietic tumor cells. Syngeneic tumor cells were lysed regardless of whether they produced infectious MuLV or expressed viral antigens gp-71, p-30, or p-12 at the cell surface. Syngeneic normal cells (thymus, lymph node, or Concanavalin A-stimulated spleen cells) used as targets in LMC assays were uneffected by lymphocytes harvested from secondary allogeneic MTLC. Several other in vitro culture treatments including secondary syngeneic MTLC and repetitive mixed lymphocyte culture stimulations were incapable of generating tumor-specific cytotoxic lymphocytes.

Based upon these results, we propose that secondary MTLC stimulation of normal spleen cells with allogeneic nonproducer leukemia cells selects for the proliferation of two subpopulations of antigen-specific cytotoxic lymphocytes. The population capable of effecting syngeneic tumor cell lysis is directed against tumor-associated cell surface antigens which may be distinct from viral structural proteins or glycoproteins. The growth of these tumor-specific cytotoxic lymphocytes may be enhanced by a soluble allogeneic effect factor produced by the proliferation of the second subpopulation of lymphocytes generated in repetitive allogeneic MTLC, namely those lymphocytes with specificities directed against differing histocompatibility antigens.
CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    What's this?

This article has been cited by other articles:

• Trifilo, M. J., Bergmann, C. C., Kuziel, W. A., Lane, T. E. (2003). CC Chemokine Ligand 3 (CCL3) Regulates CD8+-T-Cell Effector Function and Migration following Viral Infection. J. Virol. 77: 4004-4014 [Abstract] [Full Text]  
• Malek, T. R., Yu, A., Scibelli, P., Lichtenheld, M. G., Codias, E. K. (2001). Broad Programming by IL-2 Receptor Signaling for Extended Growth to Multiple Cytokines and Functional Maturation of Antigen-Activated T Cells. J. Immunol. 166: 1675-1683 [Abstract] [Full Text]  
• Odaka, C., Mizuochi, T. (1999). Role of Macrophage Lysosomal Enzymes in the Degradation of Nucleosomes of Apoptotic Cells. J. Immunol. 163: 5346-5352 [Abstract] [Full Text]  
• Leung, B. L., Haughn, L., Veillette, A., Hawley, R. G., Rottapel, R., Julius, M. (1999). TCR{alpha}{beta}-Independent CD28 Signaling and Costimulation Require Non-CD4-Associated Lck. J. Immunol. 163: 1334-1341 [Abstract] [Full Text]  
• Saito, N. G., Chang, H.-C., Paterson, Y. (1999). Recognition of an MHC Class I-Restricted Antigenic Peptide Can Be Modulated by para-Substitution of Its Buried Tyrosine Residues in a TCR-Specific Manner. J. Immunol. 162: 5998-6008 [Abstract] [Full Text]  
• Smith, K. (1988). Interleukin-2: inception, impact, and implications. Science 240: 1169-1176 [Abstract]  
• Mohapatra, S., Pledger, W. J. (2001). Interdependence of cdk2 Activation and Interleukin-2Ralpha Accumulation in T Cells. J. Biol. Chem. 276: 21984-21989 [Abstract] [Full Text]  

Home | Help | Feedback | Subscriptions | Archive | Search

TABLE OF CONTENTS