Lisa C. Osborne

TL;DR: It is found that embryonic precursor cells seeded the intestinal mucosa and demonstrated extensive in situ proliferation during the neonatal period, but these cells did not persist in the intestine of adult mice and were replaced around the time of weaning by the chemokine receptor CCR2–dependent influx of Ly6Chi monocytes that differentiated locally into mature, anti-inflammatory macrophages.

TL;DR: It is demonstrated that antibiotic-treated ABX mice exhibit impaired innate and adaptive antiviral immune responses and substantially delayed viral clearance after exposure to systemic LCMV or mucosal influenza virus, indicating that commensal-derived signals provide tonic immune stimulation that establishes the activation threshold of the innate immune system required for optimal antiviral immunity.

TL;DR: It is shown that tuft cells, which are taste-chemosensory epithelial cells, accumulate during parasite colonization and infection and are identified as critical sentinels in the gut epithelium that promote type 2 immunity in response to intestinal parasites.

TL;DR: Recent advances in understanding of the AREG-EGF receptor pathway and its involvement in infection and inflammation are discussed and a model for the function of this pathway in the context of resistance and tissue tolerance is proposed.

TL;DR: A previously unrecognized pathway of innate immune cell-mediated tissue protection in which IL-33 ameliorated disease through induction of ILC2s and the growth factor amphiregulin (AREG) is revealed, demonstrating a critical feedback loop in which cytokine cues from damaged epithelia activate innate immune cells to express growth factors essential for ILC-dependent restoration of epithelial barrier function and maintenance of tissue homeostasis.