Recruitment of T effector cells into sites of inflammation

Journal/Book: Z Rheumatol 1999; 58: 377. 1999;

Abstract: Prof. Dr. A. Hamann; Experimentelle Rheumatologie Medizinische Klinik Charité Humboldt-Universität Berlin und Deutsches Rheumaforschungszentrum (DRFZ) Berlin Recruited effector cells play an important role in the pathophysiology of autoimmune reactions. Upon inflammation endothelium and tissue cells are induced by various mediators to express adhesion molecules and to produce chemokines. This leads to an increased recruitment of effector cells into the inflamed tissue. The kind of tissue is of importance and most likely also the type and stage of inflammation. The spectrum of adhesion molecules and of chemokines involved depends on these factors. However the specificity e.g. for distinct tissues is less strict than thought before and the adhesion pathways used are largely overlapping. On the side of T cells selectivity in migration into tissues and inflamed sites is regulated too; it depends on subset activation- and differentiation state. Whereas naive T cells recirculate well through lymphoid tissues their capacity to enter inflamed sites is poor. Induction of ligands for endothelial selectins and upregulation of integrins such as a4ß7 upon activation and differentiation into effector cells enables those cells to seek inflammatory sites. In DTH-like lesions induced by skin sensitization endothelial selectins and their ligands on T cells are key determinants of selective entry of subsets of effector cells. This pathway also plays a major role in immigration of T cells into the inflamed synovium; it is however less required for entry into the inflamed gut. Similar relative contributions are found for LFA-1. a4-Integrins are very important for mucosal sites are also involved in the recruitment into the synovia but not necessary for entry of T effector cells into the inflamed skin. ... le

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