Diet-mediated constitutive induction of novel IL-4+ ILC2 cells maintains intestinal homeostasis in mice

Abstract

Group 2 innate lymphoid cells (ILC2s) expressing IL-5 and IL-13 are localized at various mucosal tissues and play critical roles in the induction of type 2 inflammation, response to helminth infection, and tissue repair. Here, we reveal a unique ILC2 subset in the mouse intestine that constitutively expresses IL-4 together with GATA3, ST2, KLRG1, IL-17RB, and IL-5. In this subset, IL-4 expression is regulated by mechanisms similar to but distinct from those observed in T cells and is partly affected by IL-25 signaling. Although the absence of the microbiota had marginal effects, feeding mice with a vitamin B1-deficient diet compromised the number of intestinal IL-4+ ILC2s. The decrease in the number of IL-4+ ILC2s caused by the vitamin B1 deficiency was accompanied by a reduction in IL-25–producing tuft cells. Our findings reveal that dietary vitamin B1 plays a critical role in maintaining interaction between tuft cells and IL-4+ ILC2s, a previously uncharacterized immune cell population that may contribute to maintaining intestinal homeostasis.

The alarmin IL33 orchestrates type 2 immune-mediated control of thymus regeneration

“…Further analysis of 4 Get mice showed that IL4 GFP expression was also detectable in thymic ILC2 (Fig. 7e), consistent with other reports describing ILC2 as a source of type 2 cytokines 26,27 in other tissues. Interestingly, ILC2 were undetectable in the thymus at 1-day post-SLI (Fig.…”