Photodynamic therapy (PDT) of tumors elicits a strong host immune response and one of its manifestations is a pronounced neutrophilia. By blocking their function prior to Photofrin-based PDT of mouse EMT6 tumors, we have identified multiple mediators whose regulated action is responsible for this neutrophilia. In addition to complement fragments (direct mediators) released as a consequence of PDT-induced complement activation, there are at least a dozen secondary mediators that all arise as a result of complement activity. The latter include cytokines IL-1beta, TNF-alpha, IL-6, IL-10, G-CSF and KC, thromboxane, prostaglandins, leukotrienes, histamine, and coagulation factors.