Thank you for visiting nature.com. You are using a browser version with limited support for CSS. To obtain
the best experience, we recommend you use a more up to date browser (or turn off compatibility mode in
Internet Explorer). In the meantime, to ensure continued support, we are displaying the site without styles
and JavaScript.
Type 1 Innate lymphoid cells (ILC1) accumulate in the inflamed mucosa of patients with Crohn’s disease (CD) but their role in CD pathogenesis remains poorly known. In a recent issue of Nature materials, Jowett et al. (Nat. Mat. 2020) used a coculture model with intestinal organoids to show that ILC1 could promote intestinal epithelial growth and tissue remodeling through an unexpected mechanism that involves the transforming growth factor 1 (TGF-β1) and the metalloproteinase MMP9.
A recent paper in Cell proposes a new role for macrophages in the distal colonic mucosa, namely the generation of balloon-like processes (BLPs) that sample luminal contents and protect epithelial cells from the toxic effects of fungal metabolites absorbed during this process. Here Allan Mowat and Calum Bain discuss the implications of these novel findings for intestinal physiology and macrophage biology, highlighting how they extend our understanding of how tissue resident macrophages can adapt precisely to the physiological needs of individual anatomical niches.
PPARγ is a critical transcriptional regulator of adipogenesis and type 2 immune responses, however until recently its role in type 2 innate lymphoid cells had not been characterised. In two papers in this issue of Mucosal Immunology, PPARγ is shown to have a dominant role in ILC2 responses, mediating IL-33-responsiveness and activation.