Functional analysis of intercellular adhesion molecule‐1‐expressing human thyroid cells

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Abstract
We have tested the potential role of thyroid cell intercellular adhesion molecule‐1 (ICAM‐1) expression by in vitro assays of cell clustering and cytotoxicity. Increased ICAM‐1 appeared within 24 h of thyroid cell stimulation with cytokines and was not inhibited by the antithyroid drug methimazole. Autologous and allogeneic lymphocyte‐thyroid cell cluster formation, assessed by flow cytometry, was reduced by about one‐third in the presence of a monoclonal antibody against ICAM‐1, regardless of whether thyroid cells were expressing basal levels of ICAM‐1 or had been stimulated with interferon‐γ. The cytotoxicity produced by interleukin 2‐stimulated allogeneic lymphocytes was not consistently inhibited by anti‐ICAM‐1 antibody, but phytohemagglutinin‐stimulated lymphocytes showed a reduction of 23% – 28% in cytotoxicity against untreated or interferon‐γ stimulated thyroid cells when the anti‐ICAM‐1 monoclonal antibody was present. Finally, thyroid cells could be infected by rhinovirus, confirming the presence of fully functional ligand. These results show that ICAM‐1 expression by thyroid cells may enhance immune cell recognition and play some role in cytotoxicity, features which could be important in the initiation or perpetuation of autoimmune thyroiditis.