Metabolic regulation of type 2 immune response during tissue repair and regeneration

Abstract

Abstract Type 2 immune responses are mediated by the cytokines interleukin (IL)-4, IL-5, IL-10, and IL-13 and associated cell types, including T helper (Th)2 cells, group 2 innate lymphoid cells (ILC2s), basophils, mast cells, eosinophils, and IL-4- and IL-13-activated macrophages. It can suppress type 1-driven autoimmune diseases, promote antihelminth immunity, maintain cellular metabolic homeostasis, and modulate tissue repair pathways following injury. However, when type 2 immune responses become dysregulated, they can be a significant pathogenesis of many allergic and fibrotic diseases. As such, there is an intense interest in studying the pathways that modulate type 2 immune response so as to identify strategies of targeting and controlling these responses for tissue healing. Herein, we review recent literature on the metabolic regulation of immune cells initiating type 2 immunity and immune cells involved in the effector phase, and talk about how metabolic regulation of immune cell subsets contribute to tissue repair. At last, we discuss whether these findings can provide a novel prospect for regenerative medicine.