At the end of the immune response, activated T-cells are cleared by apoptosis. T-cell apoptosis induced by cytokine deprivation can be inhibited by the addition of exogenous cytokines or by a fibroblast-derived survival factor. Under normal circumstances, fibroblast-mediated T-cell survival may allow persistence of a small number of primed T-cells in tissues, which can be reactivated to initiate a secondary immune response. In abnormal situations, fibroblast-mediated T-cell survival may lead to the persistence of large numbers of T-cells producing a chronic inflammatory state. Evidence derived from wound healing suggests that a bidirectional interaction is possible, and T-cells are also capable of regulating fibroblast behaviour. Persistent T-cells in the wound site thus prolong a scarring response. Potential manipulation of these interactions would provide a novel strategy for developing new therapeutic interventions. For example, administration of the fibroblast survival factor that inhibits T-cell apoptosis may prolong lymphocyte survival in lymphopenic states such as AIDS. Inhibition of the survival factor on the other hand not only has potential in the treatment of chronic inflammatory states, but may also be of value in regulating scar formation with implications for the treatment of many diseases.