Regulation of ICAM-1 Expression on Human Thyroid Follicular Cells

Abstract

The finding that thyroid follicular cells affected by autoimmune disorders, i. e., Graves’ disease and Hashimoto’s thyroiditis show increased levels of HLA class I and de novo expression of class II [1,2] suggested that the target cells can play a role in the initiation and/or perpetuation of the autoimmune responses [3]. Central to this line of thinking was the model of antigen presentation in which HLA class II molecules present peptides to the helper T cells. In recent years advances in the understanding of the recognition of antigens by T cells have shown that this process is more complex. Among the newly recognized interactions between the T-lymphocytes and the target and/or antigen-presenting cell, the pair of ligands lymphocyte function antigen-1/intercellular adhesion molecule 1 (ICAM-1) seemed to play a decisive role in the initial adhesion process that enables the T cell receptor to interact with its antigen. Because of its possible involvement in the interaction between the autoreactive T cells and the thyroid follicular cells, we have studied the modulation of ICAM-1 expression in primary cultures of nonautoimmune thyroid glands.