Intestinal Immune Imbalance is an Alarm in the Development of IBD

Figure 1

The factors of the innate immune system, adaptive immune system, genetic alterations, impaired autophagy, imbalance of energy metabolism (such as lipid metabolism, glucose metabolism, and amino acid metabolism), and electrolyte disorders interact in complex manners, which ultimately cause intestinal immune imbalance and trigger the onset of IBD. The red font indicates upregulation, while the blue font indicates downregulation. Abbreviations: ILCs, innate lymphocytes; NKT, natural killer T; IEC, intestinal epithelial cell; MIP3, macrophage inflammatory protein 3; NOD2, nucleotide-binding and oligomerization domain 2; Phox2b, paired-like homeobox 2b; Atg16l1, autophagy-related 16-like 1; XIAP, X-linked inhibitor of apoptosis; NPC1, Niemann–Pick disease type C1; MTMR3, myotubularin-related protein 3; IRGM, immunity-related GTPase M; GPR65, G-protein coupled receptor 65; PUFAs, polyunsaturated fatty acids; PPARγ, peroxisome proliferator-activated receptor γ; SCFAs, short-chain fatty acids; G6PC3, glucose-6-phosphatase catalytic subunit 3; DPP-4, dipeptidyl peptidase 4; GLP-1, glucagon-like peptide 1; AhR, aryl hydrocarbon receptor.