Figure 5.

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].