[Cytokins and adhesion molecules in Graves's disease]

The course of thyroid autoimmune diseases is associated with the inflow of lymphocytes to the thyroid gland and with the expression of anti-TSH receptor, anti-thyroglobulin and antithyroid peroxidase antibodies. Vascular endothelium of the thyroid, which is not only the source of cytokines but also a location for adhesion molecules, plays a key role in the immune process. These microscopic glycoproteins participate in cell adhesion and transmission of intercellular information, which eventually leads to their activation or proliferation. Strongly expressed molecules within thyroid endothelium are involved in lymphocyte homing in the autoimmune process. A special role is assigned to ICAM and VCAM, which interact with lymphocytes or rather with integrins LFA-1 and VLA-4 present on their surface and responsible for adhesion and inflow of these cells to the sites of inflammation. The increased expression of adhesion molecules on endothelium is caused by the activation of locally produced cytokines (TNF-alpha, INF-gamma, IL-1, IL-6, sIL-6R), which are released during the inflammatory process. Such induction promotes migration of cells through endothelium during inflammation and contributes to the phasic inflow of various populations of leucocytes.