Complement upregulation in photodynamic therapy-treated tumors: Role of Toll-like receptor pathway and NFκB

Recent investigations have established that complement activation is induced following treatment of solid tumors by photodynamic therapy (PDT). The present study using mouse SCCVII tumor model affirms the proficiency of tumor-associated macrophages (TAMs) to produce complement proteins upon receiving signals such as Hsp70 released from PDT-treated cancer cells. Such communication is shown to trigger signaling involving Toll-like receptors (TLR) 2 and 4 and the activation of transcription factor NFκB leading to complement protein production. This example of complement system regulation by TLRs adds to a growing awareness of cross-talk within these two key components of innate immunity.