Immune dysfunction associated with graft-versus-host reaction in mice transplanted across minor histocompatibility barriers. I. Depressed antigen-specific antibody responses to bacteriophage phi chi 174
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Updated: Aug 15, 2026

Induction of Graft-versus-host Disease and In Vivo T Cell Monitoring Using an MHC-matched Murine Model
Published on: August 29, 2012
1Department of Biological Structure, School of Medicine, University of Washington, Seattle 98195.
The effect of the graft-versus-host reaction in response to minor histocompatibility antigens on the antibody response to a T-dependent antigen was studied in four strains of mice. Lethally irradiated mice were transplanted with bone marrow plus graded numbers of spleen cells from H-2-compatible donors. Recipients of syngeneic bone marrow transplants and recipients of allogeneic bone marrow depleted of T cells made normal antibody responses to bacteriophage phi chi 174 when immunized on day 28 (primary) and day 56 (secondary) after marrow transplantation. Recipients of allogeneic bone marrow plus spleen cells made only small amounts of specific antibody and failed to make IgG antibody after secondary immunization. The pattern of the depressed antibody response suggests that the primary mechanism of immune dysfunction in mice with the minor antigen GVHR is a lack of T helper cell function.
The effect of the graft-versus-host reaction in response to minor histocompatibility antigens on the antibody response to a T-dependent antigen was studied in four strains of mice. Lethally irradiated mice were transplanted with bone marrow plus graded numbers of spleen cells from H-2-compatible donors. Recipients of syngeneic bone marrow transplants and recipients of allogeneic bone marrow depleted of T cells made normal antibody responses to bacteriophage phi chi 174 when immunized on day 28 (primary) and day 56 (secondary) after marrow transplantation. Recipients of allogeneic bone marrow plus spleen cells made only small amounts of specific antibody and failed to make IgG antibody after secondary immunization. The pattern of the depressed antibody response suggests that the primary mechanism of immune dysfunction in mice with the minor antigen GVHR is a lack of T helper cell function.

