Fig. 1: Potential mechanisms for helminth detection by the host.
From: “Every cell is an immune cell; contributions of non-hematopoietic cells to anti-helminth immunity”
1. Established evidence indicates that helminth-induced type 2 inflammation is initiated by alarmins (IL-25, IL-33, and TSLP) and DAMPs released by dying epithelial cells. 2. However, recent evidence suggests that tuft cells (TC), specialized chemosensory cells in mucosal barriers may potentially respond to helminth-derived signals or metabolites from a helminth-altered microbiome, which causes TC release of IL-25 and cysLT. 3. There is also evidence suggesting that stromal cell (SC) niches can trigger type 2 inflammation by an IL-33-dependent mechanism. However, it is unclear if IL-33 is released by SC, either while still alive (teal) or during cellular death (gray). 4. Cholinergic neurons (Neu) exposed to helminth-derived products in vitro can release the neuropeptide NMU. But, it is unclear if neighboring cells (e.g., TC) can signal to neurons during helminth infection.
