The mechanism by which T cells signal other T cells is not well defined. This was investigated by studying the ability of circulating T cells to induce the proliferation of autologous T cell clones. Peripheral blood T cells activated by cross‐linking of the CD3/T cell receptor complex, which increased the expression of cell adhesion molecules LFA‐1, LFA‐3 and ICAM‐1, induced the proliferation of autologous T cell clones. Irradiated antigen‐activated peripheral blood T cells could also induce the proliferation of T cell clones which could not recognize that antigen. T‐T cell activation required cell contact, was not major histocompatibility complex (MHC) restricted and was blocked by monoclonal antibodies directed against adhesion molecules CD2 and LFA‐3 but was not blocked by antibody to class II MHC determinants. As CD2 is the natural ligand for LFA‐3, increased expression of T cell surface adhesion molecules LFA‐1, ICAM‐1 and particularly LFA‐3 during an inflammatory response may rapidly recruit T cells that are activated through the CD2 pathway. These results allow a simplified model to explain how relatively few antigen/MHC‐specific T cells can recruit large numbers of non‐antigen‐specific T cells in the generation of an inflammatory response and postulates a novel role of the CD2 molecule in T cell immune function.