Maternally induced graft-vs-host disease to minor antigens as a possible etiology of an acquired immunodeficiency syndrome in mice.
It has been postulated that an acquired immunodeficiency syndrome develops in neonates as the result of a maternally induced graft-vs-host disease (GVHD) that develops when sufficient numbers of maternal lymphocytes are transferred to the fetus across the placental barrier. The present study was done to determine whether major histocompatibility complex (MHC) antigens or non-MHC minor histocompatibility antigens (MiHA) were involved. Female C57BL/6 mice were bred to males of eight selected strains such that maternal-fetal disparity existed at MHC antigens and/or minor histocompatibility antigens. Offspring were tested for immune function at 6-7 weeks of age using a Jerne plaque assay to measure the humoral response to that T dependent antigen sheep red blood cells (SRBC). None of the offspring developed clinical signs of GVHD, but 3 of 124 mice tested made no immune response to SRBC. Immunodeficiency was associated with maternal-fetal disparity only at a small number of MiHA and not at the MHC. We postulate that immunodeficiency in this model is mediated by a subclinical maternally induced GVHD to paternally derived MiHA of the fetus.
Hamilton
M S
MS
Department of Biological Structure, University of Washington, Seattle.
Becker
J
J
Hamilton
B L
BL
D000163:Acquired Immunodeficiency Syndrome / Q000209:etiology*; D000818:Animals; D005260:Female; D006086:Graft vs Host Disease / Q000276:immunology*; D007112:Immunity, Maternally-Acquired; D008285:Major Histocompatibility Complex; D008297:Male; D008431:Maternal-Fetal Exchange; D051379:Mice; D008810:Mice, Inbred C57BL; D008912:Minor Histocompatibility Loci; D011247:Pregnancy