Shedding of Soluble Receptor for Tumor Necrosis Factor Alpha Induced by M. leprae or LPS from Human Mononuclear Cells

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Cell surface expression and release of the tumor necrosis factor receptor (TNFR type I) was analyzed after stimulation of peripheral blood mononuclear cells (PBMC) with <I>Mycobacterium leprae</I> (<I>M. leprae</I>) or lipopolysaccharide (LPS). A transient spontaneous expression of TNFR type I on the surface of PBMC was observed. Two hr after activation with LPS, a significant reduction of TNFR type I expression was detected: Release of TNFR type I by <I>M. leprae</I> or LPS-stimulated PBMC was evaluated with an enzyme-linked immunoabsorbent assay. This release occurred relatively later (20 to 40 hr) than the secretion of TNF alpha which reached high levels between 8 to 20 hr after activation. <BR>Thalidomide, a potent drug for the treatment of erythema nodosum leprosum episodes by inhibiting TNF alpha production, had no influence on the TNFR type I expression. Similar results were obtained with pentoxifylline. <BR>It is concluded that the release of TNFR type I by <I>M. leprae</I> or LPS-stimulated PBMC may counteract the pro-inflammatory activities of TNF alpha, by reducing the systemic toxicity of this cytokine in leprosy.

収録刊行物

  • 日本ハンセン病学会雑誌 = Japanese journal of leprosy

    日本ハンセン病学会雑誌 = Japanese journal of leprosy 68(3), 185-193, 1999-11-30

    Japanese Leprosy Association

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各種コード

  • NII論文ID(NAID)
    10008625826
  • NII書誌ID(NCID)
    AN10559906
  • 本文言語コード
    ENG
  • 資料種別
    ART
  • ISSN
    13423681
  • データ提供元
    CJP書誌  J-STAGE 
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