Open AccessLeukemogenesis, immune responsiveness, and murine leukemia virus expression in congenic AKR/J mice differing at H-2
Author(s) -
David A. Johnson,
H. G. Bedigian,
Marianna Cherry,
Hans Meier
Publication year - 1980
Publication title -
infection and immunity (print)
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.29.3.1007-1012.1980
Subject(s) - congenic , biology , leukemia , murine leukemia virus , virus , virology , immune system , antibody , rickettsia , antigen , microbiology and biotechnology , immunology , gene , genetics
In this study we examined the leukemia incidence, ectropic and xenotropic murine leukemia virus expression, and immune responsiveness of congenic AKR/J mice differing at the H locus. Congenic AKR.L-H-2b/1 mice, bearing the H-2b haplotype derived from C57L/J, were found to have a significant delay in time of death due to leukemia relative to that of AKR/J (H-2k) mice. The expression of ecotropic murine leukemia virus was found to be identical in both strains. The expression of xenotropic murine leukemia virus did vary, however, with the AKR.L-H-2b/1 mice showing a significantly reduced level of virus expression relative to AKR/J mice. In addition to these observations, we found that the AKR.L-H-2b/1 mice have an enhanced blastogenic responsiveness to phytohemagglutinin and to specific antigen to which they had previously been sensitized. Concomitant enhanced antibody response was not found. We suggest that the stronger cellular response, relative to AKR/J, may contribute to the delay in leukemia onset and to reduced xenotropic virus expression observed with the congenic mice.