Hereditary Immunodeficiency and Leukemogenesis in HRS/J Mice

摘要: Summary Adult and fetal tissues of hairless ( hr/hr ) haired hr /+, +/+) HRS/J mice contain the same or a similar amount endogenous murine C-type RNA virus. However, onset leukemia is earlier its incidence somewhat greater in than mice. This finding raises question whether mutation exerts pleiotropic effect leading to immunodeficiency, thus rendering more susceptible development normal Several different experimental approaches yielded following results. A severe thymic cortical atrophy was observed beginning at about 6 months age, with concurrent increase splenic lymphoid elements. b Whole-body DNA turnover as well DNA, RNA, protein thymus, spleen, lymph nodes, bone marrow were all three genotypes, independent age sex. c In two vivo test systems, phytohemagglutinin stimulation plaque assays for sheep red cell hemolysis, mutant responded better +/+ /+ animals. d contrast, intact mice, ability produce antibody tetanus toxoid form aluminum-adsorbed, fluid, complexed (in slight antigen excess) greatly reduced mutants. These findings indicate relative functional defect immune system these If deficient “collaboration” among types deficiency proliferative capacity immunocompetent cells occurs mutants, it may result an ineffective immunosurveillance against leukemogenesis.