Until recently, the cysteinyl leukotrienes, initially termed, slow reacting substance of anaphylaxis, were viewed entirely as effectors of smooth muscle constriction of bronchial airways to impair air flow and of microvasculature to evoke a plasma leak. The development of mice with targeted disruption of the synthesis of the cysteinyl leukotrienes or of their receptor-mediated action has within the last 5 years uncovered new functions in chronic inflammation and in regulation of the adaptive immune response. As innate host responses precede antigen presentation and then follow antigen specific recognition, it is not surprising that we find that the cysteinyl leukotrienes are implicated in both afferent and efferent cell-based immune responses, chronic inflammatory cell responses, and, as originally recognized, in acute smooth muscle constriction.