Linked Life Data

3119228

Source:http://linkedlifedata.com/resource/pubmed/id/3119228

Statements in which the resource exists.
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pubmed-article:3119228pubmed:abstractTextImmunosuppression 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 F1 hybrids (AJ----B6AF1), while the second model utilized GVHD induced across minor histocompatibility barriers (B10.D2----BALB/c). Results indicated that significant levels of serum IFN-alpha/beta are present in mice undergoing chronic GVHD. Spleen cells from chronic GVHD mice were also shown to produce significant levels of IFN-alpha/beta upon in vitro culture in medium only. This IFN-alpha/beta production was greatly increased when GVHD spleen cells were cultured with either concanavalin A (Con A) or IL-2. In contrast, IFN-gamma production was undetectable in these Con A- or IL-2-containing cultures. Additionally, these same spleen cells which produced high levels of IFN-alpha/beta were immunosuppressed as measured by mitogen-induced cell proliferation. These results suggest that IFN-gamma production is defective in GVHD spleen cells, and that the presence of high IFN-alpha/beta production by GVHD mice may contribute to the immunosuppression associated with chronic GVHD.lld:pubmed
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pubmed-article:3119228pubmed:volume110lld:pubmed
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pubmed-article:3119228pubmed:pagination120-30lld:pubmed
pubmed-article:3119228pubmed:dateRevised2008-11-21lld:pubmed
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pubmed-article:3119228pubmed:year1987lld:pubmed
pubmed-article:3119228pubmed:articleTitleEnhanced interferon-alpha/beta (IFN-alpha/beta) and defective IFN-gamma production in chronic graft versus host disease: a potential mechanism for immunosuppression.lld:pubmed
pubmed-article:3119228pubmed:affiliationDepartment of Microbiology, University of Texas Medical Branch, Galveston 77550.lld:pubmed
pubmed-article:3119228pubmed:publicationTypeJournal Articlelld:pubmed
pubmed-article:3119228pubmed:publicationTypeComparative Studylld:pubmed
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