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Research Article Free access | 10.1172/JCI4992

Donor-derived interferon gamma is required for inhibition of acute graft-versus-host disease by interleukin 12.

Y G Yang, B R Dey, J J Sergio, D A Pearson, and M Sykes

Bone Marrow Transplantation Section, Transplantation Biology Research Center, Surgical Service, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02129, USA.

Find articles by Yang, Y. in: JCI | PubMed | Google Scholar

Bone Marrow Transplantation Section, Transplantation Biology Research Center, Surgical Service, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02129, USA.

Find articles by Dey, B. in: JCI | PubMed | Google Scholar

Bone Marrow Transplantation Section, Transplantation Biology Research Center, Surgical Service, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02129, USA.

Find articles by Sergio, J. in: JCI | PubMed | Google Scholar

Bone Marrow Transplantation Section, Transplantation Biology Research Center, Surgical Service, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02129, USA.

Find articles by Pearson, D. in: JCI | PubMed | Google Scholar

Bone Marrow Transplantation Section, Transplantation Biology Research Center, Surgical Service, Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02129, USA.

Find articles by Sykes, M. in: JCI | PubMed | Google Scholar

Published December 15, 1998 - More info

Published in Volume 102, Issue 12 on December 15, 1998
J Clin Invest. 1998;102(12):2126–2135. https://doi.org/10.1172/JCI4992.
© 1998 The American Society for Clinical Investigation
Published December 15, 1998 - Version history
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Abstract

We have demonstrated that a single injection of interleukin (IL)-12 on the day of bone marrow transplantation (BMT) inhibits acute graft-versus-host disease (GVHD) in mice. This effect of IL-12 can be diminished by anti-interferon (IFN)-gamma mAb. To determine the mechanism by which IFN-gamma affects IL-12-mediated GVHD protection, we have compared the effect of IL-12 on GVHD in C57BL/6 wild-type (WT) or IFN-gamma gene knockout (GKO) recipients of fully major histocompatibility complex plus minor antigen-mismatched allogeneic BMT from WT or GKO BALB/c mice. Lethal acute GVHD was readily induced in the absence of IFN-gamma. IL-12 inhibited GVHD mortality to a similar extent in WT and GKO recipients of WT allogeneic BMT. However, neither WT nor GKO recipients were protected by IL-12 from GVHD induced by GKO allogeneic BMT. Moreover, the effective inhibition of host-reactive donor T cell activation and expansion that is associated with IL-12-mediated GVHD protection was dependent on the ability of BALB/c donors to produce IFN-gamma. These results demonstrate that (a) acute GVHD can be induced in the absence of IFN-gamma, (b) host IFN-gamma does not play a critical role in IL-12-induced GVHD protection, and (c) the protective effect of IL-12 against GVHD is dependent on the ability of the donor to produce IFN-gamma.

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  • Version 1 (December 15, 1998): No description

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