Hong-Erh Liang

TL;DR: The findings suggest a mechanism by which diverse perturbations can activate type 2 immunity and reveal a shared local-tissue-elicited checkpoint that can be exploited to control both innate and adaptive allergic inflammation.

TL;DR: Dendritic cell activation by Listeria nucleated rapid clustering of innate cells, including granulocytes, natural killer (NK) cells, and monocytes, to sites of bacteria propagation where interleukin-12 was expressed in the spleen, which restricts pathogens before adaptive immunity is fully activated.

TL;DR: This work provides comprehensive temporally controlled fate mapping of an innate lymphocyte subset with notable nuances as compared to tissue macrophage ontogeny and shows that perinatal ILC2s were variably replaced across tissues with age.

TL;DR: Extrahepatic arginase-1+ Id2+ fetal ILC precursors that express a transitional developmental phenotype (ftILCPs) and differentiate into ILC1s, ILC2s and ILC3s in vitro are identified and reside in the intestine during PP development, where they aggregate at PP anlagen after stromal cell activation and become a localized source of ILC populations.

TL;DR: It is shown that tuft cells secrete cysteinyl leukotrienes (cysLTs) to rapidly activate type 2 immunity following chemosensing of helminth infection, and context-specific regulation of tuft-ILC2 circuits within the small intestine is suggested.