Mechanism of immune dysfunction associated with minor antigen graft-vs-host disease in mice.
A well-characterized murine model of graft-vs-host disease (GVHD) that develops in response to minor histocompatibility antigens was used to study the mechanism of an immunodeficiency syndrome that is associated with GVHD. Lethally irradiated mice were transplanted with a combination of bone marrow and spleen cells from H-2 compatible donors that differed at multiple minor histocompatibility antigens, or from syngeneic donors. Four to 12 weeks later, the humoral responses of transplanted and control mice to the T dependent antigens bacteriophage phiX174 and TNP-sheep red blood cells (TNP-SRBC), and to the T independent antigen TNP-Brucella abortus (TNP-BA) were determined. The results demonstrate that mice with GVHD have relatively intact B Cell function and a profound defect in T helper cell function. The immune response to T dependent antigens normalized with repeated immunization. We conclude that immune dysfunction in mice with GVHD is due to a reversible defect in T helper cell function.
Hamilton
B L
BL
Department of Biological Structure, University of Washington, Seattle.
Budhecha
S
S
Hamilton
M S
MS
Ochs
H D
HD
D000818:Animals; D000917:Antibody Formation; D000955:Antigens, T-Independent / Q000494:pharmacology; D001402:B-Lymphocytes / Q000276:immunology; D006086:Graft vs Host Disease / Q000276:immunology*; D007117:Immunization, Secondary; D051379:Mice; D008912:Minor Histocompatibility Loci; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology
D000955:Antigens, T-Independent