Expression of intercellular adhesion molecule-1 (ICAM-1) on human thyroid cells lines correlated with their binding

P D Fowler1, M Tacker, G S Whitley

  • 1Department of Cellular and Molecular Sciences, St. George's Hospital Medical School, London, U.K.

Insights

Human thyroid cells express intercellular adhesion molecule-1 (ICAM-1), which is upregulated by cytokines. Lymphocyte binding to these cells involves ICAM-1 and lymphocyte function-associated antigen-1 (LFA-1).

Area of Science:

  • Immunology
  • Cell Biology
  • Endocrinology

Background:

  • Intercellular adhesion molecule-1 (ICAM-1) plays a role in immune cell interactions.
  • Thyroid cells' immune response mechanisms are not fully understood.
  • Novel human thyroid cell lines (SGHTL) provide a model for studying thyroid cell behavior.

Purpose of the Study:

  • To investigate ICAM-1 expression in human thyroid cells.
  • To determine the role of ICAM-1 in lymphocyte adhesion to thyroid cells.
  • To elucidate the molecular pathways involved in thyroid cell-lymphocyte interactions.

Main Methods:

  • Utilized novel functional human thyroid cell lines (SGHTL).
  • Analyzed ICAM-1 expression using cytokine stimulation (gamma-interferon, interleukin-1, tumor necrosis factor).
  • Assessed lymphocyte binding to thyroid cells and inhibition using monoclonal antibodies against ICAM-1, LFA-1, CD2, and MHC class II antigens.

Main Results:

  • ICAM-1 is constitutively expressed on SGHTL cells and rapidly upregulated by recombinant cytokines.
  • Major histocompatibility complex (MHC) class II antigens showed slower upregulation by gamma-interferon.
  • Activated lymphocyte binding to SGHTL cells increased after cytokine treatment and was inhibited by anti-ICAM-1 and anti-LFA-1 antibodies.

Conclusions:

  • Thyroid cell binding of lymphocytes involves an LFA-1 and ICAM-1 dependent pathway.
  • Cytokine-induced upregulation of ICAM-1 enhances lymphocyte adhesion.
  • The interaction does not appear to involve MHC class II antigens or CD2.