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Enhanced interferon-α/β (IFN-α/β) and defective IFN-γ production in chronic graft versus host disease: a potential mechanism for immunosuppression
Journal article   Peer reviewed

Enhanced interferon-α/β (IFN-α/β) and defective IFN-γ production in chronic graft versus host disease: a potential mechanism for immunosuppression

Mark G Cleveland, Richard G Lane and Gary R Klimpel
Cellular immunology, Vol.110(1), pp.120-130
11/01/1987
DOI: 10.1016/0008-8749(87)90106-7
PMID: 3119228

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Abstract

Immunosuppression is a well-characterized consequence of chronic graft-versus-host disease (GVHD). We have previously shown that interferon (IFN) is produced in high levels during acute GVHD. Our objective in this study was to determine if IFN, as a cytokine with known immunosuppressive qualities, could be detected in mice experiencing chronic GVHD-induced immunosuppression. Two different experimental models were used to induce chronic GVHD. The first model involved the injection of parental strain spleen cells into adult F, hybrids (AJ -+ B6AF,), while the second model utilized GVHD induced across minor histocompatibility barriers (BlO. D2 -+ BALB/c). Results indicated that significant levels of serum IFN-α/β are present in mice undergoing chronic GVHD. Spleen cells from chronic GVHD mice were also shown to produce significant levels of IFN-α/β upon in vitro culture in medium only. This IFN-α/β production was greatly increased when GVHD spleen cells were cultured with either concanavlin A (Con A) or IL-2. In contrast, IFN-y production was undetectable in these Con A- or IL-2- containing cultures. Additionally, these same spleen cells which produced high levels of IFN- α/β were immunosuppressed as measured by mitogen-induced cell proliferation. These results suggest that IFN-y production is defective in GVHD spleen cells, and that the presence of high IFN-α/β production by GVHD mice may contribute to the immunosuppression associated with chronic GVHD.
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