Lymphoblastoid interferon-α inhibits T cell proliferation and expression of eosinophil-activating cytokines

Guha Krishnaswamy, John K. Smith, Sujata Srikanth, David S. Chi, John H. Kalbfleisch, Shau Ku Huang

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36 引文 斯高帕斯(Scopus)

摘要

T cell-derived cytokines, such as interleukin-5 (IL-5) and granulocyte- macrophage colony-stimulating factor (GM-CSF) activate eosinophils, whereas other cytokines, such as tumor necrosis factor (TNF)-α and IL-13, determine eosinophil recruitment. Interferon-α (IFN-α), a leukocyte-derived cytokine, has been shown to have beneficial effects in eosinophil-mediated disorders, such as the hypereosinophilic syndrome and a murine model of allergic asthma, where it inhibited eosinophil recruitment. We tested the hypothesis that IFN- α acted in eosinophil-mediated disorders by modulating T cell cytokine expression. Peripheral blood mononuclear cells (PBMC) or human ragweed- specific T(H1) (2B8) and T(H2) (2D2) T cell clones were cultured in the presence of 5 μg/ml of phytohemagglutinin (PHA) or 25 μg/ml of antigen Amb a 1 (short ragweed allergen), respectively, and lymphoblastoid IFN-α (varying from 0 to 10,000 U/ml). We assessed T cell proliferation by [3H]thymidine incorporation and production of IL-5 and GM-CSF by ELISA. Expression of cytokine transcripts was analyzed by the reverse transcription- polymerase chain reaction technique (RT-PCR). IFN-α induced a dose-dependent suppression of T cell proliferation of both PBMC (p < 0.001) and the T cell clones (p < 0.001). IFN-α inhibited gene expression of IL-5, GM-CSF, TNF- α, and IL-13 in PBMC. Furthermore, IFN-α significantly inhibited mitogen- induced and antigen-induced production of IL-5 and GM-CSF. IFN-α may benefit eosinophil-mediated disorders by inhibiting T cell function and production of cytokines active on human eosinophils.

原文英語
頁(從 - 到)819-827
頁數9
期刊Journal of Interferon and Cytokine Research
16
發行號10
DOIs
出版狀態已發佈 - 一月 1 1996
對外發佈Yes

ASJC Scopus subject areas

  • Immunology
  • Cell Biology
  • Virology

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