In April, Chris Medina, from CIC faculty member, Kodi Ravichandran’s lab successfully defended his thesis “Intercellular metabolite communication via Pannexin 1 coordinates inflammation.” He focused on how pannexin 1 channels regulate inflammatory responses in two different settings: the process of apoptosis, and the function of T regulatory cells.
He describes one mechanism by which apoptotic cells can orchestrate the specific release of metabolites. Such extracellular metabolites, in turn, are able to signal to the surrounding cells to maintain an anti-inflammatory state within the tissue and could be harnessed for therapeutic potential. In the second part of this dissertation, Medina describes a novel mechanism by which Teff and Treg cells can communicate via extracellular adenine nucleotides. This occurs to optimally mediate suppression of the immune response by Treg cells and this crosstalk was dependent on Panx1 channels. Collectively, the data suggests novel mechanisms by which apoptotic cells and Panx1 can mediate intercellular communication between cells which is important for the proper control of inflammation.