Pulmonary and Critical Care Medicine Fellow Northwestern Univ. Chicago, Illinois, United States
Disclosure(s):
Benjamin J. Ulrich, MD, PhD: No financial relationships to disclose
Introduction/Rationale: Pneumonia triggers inflammatory responses followed by recovery and tissue repair. T regulatory (Treg) cells play a necessary role in coordinating the recovery process. Amphiregulin (Areg) is an epidermal growth factor receptor ligand that mediates the lung tissue-reparative function of Treg cells in mice. While IL-18 receptor and ST2 signaling promote Areg secretion from Treg cells, the signals required for optimal Areg production are unclear.
Methods: Mice were inoculated with influenza A with examination of lung and spleen Treg cells during the recovery phase of pneumonia.
Results: Here, we show in a model of influenza A pneumonia that Areg expression in lung and spleen Treg cells does not require paracrine or autocrine signaling following restimulation. Furthermore, optimal Areg detection required nuclear permeabilization, indicating that Areg may be localized within the nucleus.
Conclusion: These findings suggest that Treg cells are intrinsically programmed to produce Areg upon activation, independent of autocrine and paracrine signaling cues. Additionally, Areg may function to regulate transcriptional programs within the nucleus of Treg cells.
