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Research Article Free access | 10.1172/JCI117453

Antibody to the ligand of CD40, gp39, blocks the occurrence of the acute and chronic forms of graft-vs-host disease.

F H Durie, A Aruffo, J Ledbetter, K M Crassi, W R Green, L D Fast, and R J Noelle

Department of Microbiology, Dartmouth Medical School, Lebanon, New Hampshire 03756.

Find articles by Durie, F. in: JCI | PubMed | Google Scholar

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

Published in Volume 94, Issue 3 on September 1, 1994
J Clin Invest. 1994;94(3):1333–1338. https://doi.org/10.1172/JCI117453.
© 1994 The American Society for Clinical Investigation
Published September 1, 1994 - Version history
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Abstract

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.

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