These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Genetic control of the induction of cytolytic T lymphocyte responses to AKR/Gross viral leukemias. I. H-2-encoded dominant gene control.
    Author: Green WR.
    Journal: J Immunol; 1984 May; 132(5):2658-64. PubMed ID: 6425409.
    Abstract:
    Previously, a system was devised whereby H-2-restricted cytotoxic T lymphocytes could be raised that were specific for tumors induced by endogenous AKR/Gross murine leukemia virus and that displayed the Gross cell surface antigen (GCSA). The generation of such anti-AKR/Gross virus CTL required in vivo priming with allogeneic (H-2 and/or non-H-2 incompatible) GCSA+ tumor cells, followed by in vitro restimulation with H-2-compatible GCSA+ tumor cells. The prototype responder strain of mice was C57BL/6, which is of the H-2b type and which has a low incidence of spontaneous virus-induced leukemia ("low leukemic"). Present experimentation indicates that there is H-2-encoded control of the ability to mount an anti-AKR/Gross virus CTL response. In addition to C57BL/6, all other H-2b strains tested, including C57BL/10, C57L, and 129, were responders. In contrast, H-2k strains of both "high leukemic" (AKR) and "low leukemic" (AKR.Fv-1b and CBA) phenotype appeared to be low- or nonresponders with respect to their ability to generate H-2k-restricted anti-AKR/Gross virus CTL after appropriate stimulation. Furthermore, B6.H-2k congenic mice were also poorly responsive, suggesting that H-2b and H-2k were responder and nonresponder haplotypes, respectively. The finding that (responder X nonresponder)F1, i.e., (B6 X CBA)F1 mice mounted CTL responses to H-2b, but not H-2k, GCSA+ tumors, was consistent with this interpretation and suggested the presence of H-2-encoded dominant immune response genes. The tumors of AKR background that were efficient in the in vivo priming of C57BL/6 mice were relatively inefficient in priming (B6 X CBA)F1 mice for a subsequent in vitro H-2b-restricted anti-AKR/Gross virus CTL response. Because of the similarities in background minor H genes of the AKR and CBA strains, this latter observation was in keeping with the requirement for in vivo stimulation with tumor cell alloantigens in addition to the virus-associated target antigens.
    [Abstract] [Full Text] [Related] [New Search]