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Differential inhibitory effects of interleukin‐10, interleukin‐4, and dexamethasone on staphylococcal enterotoxin‐induced cytokine production and T cell activation
Author(s) -
Krakauer Teresa
Publication year - 1995
Publication title -
journal of leukocyte biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.819
H-Index - 191
eISSN - 1938-3673
pISSN - 0741-5400
DOI - 10.1002/jlb.57.3.450
Subject(s) - cytokine , peripheral blood mononuclear cell , tumor necrosis factor alpha , biology , immunology , interferon gamma , interleukin , dexamethasone , interleukin 10 , t cell , interleukin 4 , endocrinology , immune system , in vitro , biochemistry
The cytokine profile of human peripheral blood mononuclear cells (PBMC) stimulated by staphylococcal enterotoxin (SE) A and B was examined. Production of tumor necrosis factor (TNFα), interleukin (IL)‐1, IL‐6, IL‐2, and gamma interferon (IFN‐γ) was observed. In contrast, Th2 cytokines IL‐4 and IL‐10 were absent from SEA‐ or SEB‐stimulated PBMC. Moreover, adding IL‐10 to SE‐stimulated PBMC inhibited the production of IL‐1, IL‐6, TNFα, and IFNγ by 50 to 80% but had less effect (8–30%) on T cell proliferation. IL‐4 was less effective than IL‐10 in inhibiting cytokine production and enhanced T cell proliferation by SEA or SEB. The antiinflammatory agent, dexamethasone, was the most potent agent in controlling the SE‐mediated effects as evidenced by inhibited T cell proliferation (55%) and reduced levels of IL‐1, IL‐6, and IFNγ (60% to 100%) and TNFα (50%). Reducing levels of toxic mediators such as TNFα, IL‐1, IL‐6, and IFNγ by dexamethasone in SE‐induced T cell responses may be a useful therapeutic strategy to circumvent SE toxicity and pathogenesis. J. Leukoc. Biol . 57: 450–454; 1995.