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The image shows the expression of protease ELA2A (green), its inhibitor ELAFIN (red) and nuclei (dapi, white) in epithelial cells from human colon biopsies. ELA2A was shown to be secreted by intestinal epithelial cells, where its hyper-activity contributes to intestinal inflammation. Photo courtesy of Anissa Edir and Céline Deraison, INSERM IRSD, Toulouse, France. For more information, please see manuscript in this issue, page 669.
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.
ILC2s are critical in the immune response to helminths, the development of allergies and homeostasis of adipose tissue. This study demonstrates that the metabolic sensor PPARγ is central for ILC2s activation, proliferation and function in lung and adipose tissue.