Schematic representation summarizing the putative signaling pathways acted upon by TTN in human PMNs. TTN likely activates G protein-coupled membrane receptors, which in turn signal to PLC- and PKC-dependent pathways. PKC may exert both positive and negative modulation of TTN signaling, eventually depending on the specific isoform involved. Increased [Ca++]i then occurs through both Ca++ release from intracellular stores and Ca++ entry, possibly through T-type Ca++ channels. The picture is based upon the results of the present as well as of previous studies [8,9].