T‐cell activation requires ‘contact’ with antigen‐presenting cells (APCs) to bring the T‐cell receptor (TCR) and antigenic major histocompatibility complex (MHC)‐peptide complex together. Contact is defined by the size of the TCR and MHC–peptide complex, which at approximately 13 nm requires extensive interdigitation of the glycocalyx of the T cell and APC. T cells may be activated through formation of a stable T cell–APC junction, referred to as an immunological synapse. It has also been shown in vitro that T cells can integrate signals from APCs without a stable interaction. In vivo imaging studies supported the importance of both motile and stable T cell–APC interactions in T‐cell priming. We have found that stability depends not upon turning off motile machinery but by symmetrization of force‐generating structures to balance forces and hold the cell in place. Motility is induced by breaking this symmetry, which may be necessary to maintain the differentiation potential of the T cell. Recently, we also discovered a mode of T‐cell signaling leading to tolerance in vivo based purely on motile interactions. Because this entire process takes place in a state of continuous T‐cell kinesis, I propose the term ‘kinapse’ for motile T cell–APC contacts leading to signaling. Synapses and kinapses are inter‐convertible by symmetrization/symmetry breaking processes, and both modes appear to be involved in normal T‐cell priming. Imbalance of synapse/kinapse states may lead to immunopathology.