T cell adhesion.

Antigen recognition by the T cell receptor cannot ensure by its own T cell activation. Other membranes molecules are required in order to achieve transient but strong adhesion of the T cell to the antigen presenting cell. Two main molecular adhesion pathways have been characterized involving the CD2 molecule binding the LFA-3 molecule and the LFA-1 molecule binding the ICAM-1 or ICAM-2 molecule. These results have been provided by the use of the three approaches, i-e inhibition of T cell activation and adhesion by monoclonal antibodies, the study of the adhesion of lymphocytes that do not express one or several adhesion molecules and finally the demonstration that the transfection of gene(s) coding for adhesion molecules into fibroblasts cotransfected with HLA molecules make the latter cells able to present antigen(s). The importance of the concept of antigen-independent T cell adhesion has been further underlined by in vivo use of monoclonal antibodies specific for adhesion molecule(s): LFA-1. Such antibody can efficiently block rejection of HLA non identical bone marrow in children. This opens further prospect of immunosuppression through blocking of T cell adhesion.