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Research Article Free access | 10.1172/JCI117453
Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.
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Published September 1, 1994 - More info
Chronic and acute graft-versus-host disease (cGVHD and aGVHD) result from donor cells responding to host disparate MHC alleles. In cGVHD (H-2d-->H-2bd), heightened polyclonal immunoglobulin production is due to the interaction of donor allospecific helper T cells (Th) and the host B cells. In vivo administration of antibody to the ligand for CD40, gp39, blocked cGVHD-induced serum anti-DNA autoantibodies, IgE production, spontaneous immunoglobulin production in vitro, and associated splenomegaly. Antibody production remained inhibited for extended periods of time after termination of anti-gp39 administration. Antiallogeneic CTL responses induced in a GVHD were also prevented by the in vivo administration of anti-gp39 as was the associated splenomegaly. These data suggest that CD40-gp39 interactions are critical in GVHD and that CD40-gp39 may be a valuable ligand-receptor pair for targeting immunotherapeutic agents to control GVHD.