Regulation of ICAM-1-mediated fibroblast-T cell reciprocal interaction: Implications for modulation of gut inflammation
Regulation of ICAM-1-mediated fibroblast-T cell reciprocal interaction: Implications for modulation of gut inflammation
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DOI：
10.1016/s0016-5085(99)70447-6
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发表时间：
1999-09-01
期刊：
影响因子：
29.4
通讯作者：
Fiocchi, C
中科院分区：
文献类型：
--
作者：
Musso, A;Condon, TP;Fiocchi, C
Background & Aims: Immune-nonimmune cell interactions modulate mucosal immunity. We investigated the expression of adhesion molecules by intestinal fibroblasts, the effect of immune cell-derived factor on fibroblast binding of T cells, and the consequences of interfering with adhesion molecule expression on fibroblast-T cell interaction. Methods: Expression of fibroblast intercellular; adhesion molecule (ICAM)-1 and vascular cell adhesion molecule (VCAM)-1 surface and messenger RNA (mRNA) was measured before and after exposure to immune cell-derived supernatants. Fibroblasts were treated with antibodies to ICAM-1 or VCAM-1, or ICAM-1 antisense oligonucleotide;lsis 2302, before a T-cell adhesion assay. Results: Fibroblast activation by immune cell-derived cytokines enhanced ICAM-1 and VCAM-1 surface expression and mRNA as well as adhesiveness for T cells. Blockade with neutralizing antibodies showed that binding was almost exclusively dependent on ICAM-1. Isis 2302 specifically reduced fibroblast ICAM-1 mRNA and dose-dependently inhibited ICAM-1 surface expression and T-cell binding. Conclusions: ICAM-1 is essential for intestinal fibroblast binding of T cells, a phenomenon that is efficiently and specifically disrupted by ICAM-1 antisense oligonucleotides, These observations emphasize the crucial regulatory role of fibroblasts in mucosal immunity and their potential as targets for therapeutic intervention in intestinal inflammation.
