THE ROLE OF ICAM-1 ON T-CELLS IN THE PATHOGENESIS OF ASTHMA

The capacity of inflammatory cells to adhere is critical to inflammato ry responses and involves an array of adhesion molecules grouped into distinct families, Intercellular adhesion molecule (ICAM)-1 has recent ly attracted much interest in view of increasing evidence that it play s a prominent role in allergic diseases such as asthma and rhinitis, A part from its role in adhesion of inflammatory cells to vascular endot helium, the extracellular matrix and epithelium, ICAM-1 mediates T-cel l/T-cell, T-cell/target cell and T-cell/B-cell interactions, ICAM-1 on the surface of T-cells is thought to participate in signal transducti on and may thus modulate several functions including activation, proli feration, cytotoxicity and cytokine production. Because ICAM-1 is the receptor for the major group of rhinoviruses, the most important cause of acute asthma attacks, binding of rhinovirus (RV) to ICAM-1 on T-ce lls may, at least theoretically, modulate their function. We review he re the role of ICAM-1 in asthma and focus more specifically on its exp ression on T-cells, We present evidence for a general increase in ICAM -1 expression in this disease including recent observations of enhance d expression on the surface of T-cells in the airways lumen. Whilst th e implications of intercellular adhesion molecule-1 upregulation in as thma remain to be fully elucidated, its participation in cell traffick ing and activation are being considered as a target for treatment. We present here early attempts to interfere with intercellular adhesion m olecule-1 as an adhesion molecule involved in cell influx and studies aimed preventing virus-induced exacerbations of asthma in children bas ed on the knowledge that intercellular adhesion molecule-1 is the rece ptor for rhinoviruses.