| First Author | Stanbery AG | Year | 2026 |
| Journal | Immunity | Volume | 59 |
| Issue | 5 | Pages | 1381-1397.e6 |
| PubMed ID | 41903550 | Mgi Jnum | J:392083 |
| Mgi Id | MGI:8323472 | Doi | 10.1016/j.immuni.2026.02.022 |
| Citation | Stanbery AG, et al. (2026) Tuft cells promote reactivation of memory Th2 cells and are required for protective immunity to intestinal helminth re-infection. Immunity |
| abstractText | Small intestinal (SI) tuft cells are critical sentinels for innate type 2 immunity against helminths, but their role in adaptive responses is unclear. We show that despite the presence of protective memory CD4(+) T helper 2 (Th2) cells, tuft cells remain essential for worm clearance during a secondary infection with Heligmosomoides polygyrus bakeri (H. polygyrus bakeri). Th2 cells still develop in the absence of tuft cells or group 2 innate lymphoid cells but upregulate receptors for tuft cell effectors interleukin-25 (IL-25) and leukotriene C(4) (LTC(4)) when they enter the SI. IL-25 and LTC(4) are sufficient to drive IL-13 production by Th2 cells, and their absence during a secondary infection diminishes IL-13. Complete restriction of a secondary H. polygyrus bakeri infection requires granulomas that reduce worm fitness together with tuft cell-dependent clearance from the intestinal lumen. Thus, tuft cells regulate both innate and adaptive immunity, and we extend the paradigm that Th2 cells require tissue-specific cues for optimal function. |
