Adhesion of T lymphoblasts to epidermal keratinocytes is regulated by interferon gamma and is mediated by intercellular adhesion molecule 1 (ICAM-1).

DOI PDF 被引用文献23件
  • M L Dustin
    Laboratory of Membrane Immunochemistry, Dana Farber Cancer Institute, Boston, Massachusetts 02115.
  • K H Singer
    Laboratory of Membrane Immunochemistry, Dana Farber Cancer Institute, Boston, Massachusetts 02115.
  • D T Tuck
    Laboratory of Membrane Immunochemistry, Dana Farber Cancer Institute, Boston, Massachusetts 02115.
  • T A Springer
    Laboratory of Membrane Immunochemistry, Dana Farber Cancer Institute, Boston, Massachusetts 02115.

抄録

<jats:p>The cell surface expression and function of the LFA-1 ligand, intercellular adhesion molecule 1 (ICAM-1), on epidermal keratinocytes (EK) was studied. ICAM-1 expression on the surface of cultured EK was either absent or weak, but was induced by treating EK with rIFN-gamma or TNF for 4-48 h. IFN-gamma and TNF were synergistic. IFN-gamma treatment increased T lymphoblast adhesion from less than 2% to 20-40%, with a concentration dependence similar to that seen for ICAM-1 induction. All of the adhesion to EK was inhibited by LFA-1 and ICAM-1 mAbs, but not by HLA-DR, CD2, or LFA-3 mAbs. There was no difference in the level of T lymphoblast adhesion to IFN-gamma-treated allogeneic or autologous EK. ICAM-1 purified from the HeLa epithelioid cell line and reconstituted into planar membranes also supported efficient adhesion of T lymphoblasts that was blocked by LFA-1 mAb bound to the T lymphoblasts or ICAM-1 mAb bound to the planar membranes. T lymphoblasts adherent to EK or ICAM-1 planar membranes were isolated by panning, and surface markers were analyzed by immunofluorescence flow cytometry. The adherent T cells were a phenotypically skewed subpopulation. They were enriched for CD8+ cells and expressed 1.5-2.5-fold higher LFA-1 and CD2 compared with the unseparated population.</jats:p>

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