IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis

Sugimoto, Ken; Ogaẃa, Atsuhiro; Mizoguchi, Emiko; Shimomura, Yoshiharu; Andoh, Akira; Bhan, Atul K.; Blumberg, Richard S.; Xavier, Ramnik J.; Mizoguchi, Atsushi

doi:10.1172/jci33194

Cited by 709 publications

(893 citation statements)

References 53 publications

(108 reference statements)

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“…Thus, IL-22 modulates local tissue responses and targets cells of the skin, the digestive tract, the lungs and the kidney and promotes cell proliferation and differentiation, thereby enhancing host defence and wound-healing responses [113]. Moreover IL-22 exhibits protective functions by limiting tissue damage during inflammatory processes of the liver [114], the gut [115,116]and the myocardium [117]. The role of IL-22 in autoimmunity is not yet clear.…”

Section: Il-22mentioning

confidence: 99%

Cytokines and effector T cell subsets causing autoimmune CNS disease

2011

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a b s t r a c tAlthough experimental autoimmune encephalomyelitis (EAE) is limited in its potency to reproduce the entirety of clinical and histopathologic features of multiple sclerosis (MS), this model has been successfully used to prove that MS like autoimmunity in the CNS is orchestrated by autoantigen specific T cells. EAE was also very useful to refute the idea that IFN-c producing T helper type 1 (Th1) cells were the sole players within the pathogenic T cell response. Rather, ''new'' T cell lineages such as IL-17 producing Th17 cells or IL-9 producing Th9 cells have been first discovered in the context of EAE. Here, we will summarize new concepts of early and late T cell plasticity and the cytokine network that shapes T helper cell responses and lesion development in CNS specific autoimmunity.

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Section: Il-22mentioning

confidence: 99%

Cytokines and effector T cell subsets causing autoimmune CNS disease

2011

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“…ILC3s are a group of lymphocytes without T‐cell‐specific antigen receptors with particular accumulation at mucosal sites and serve as key regulators during intestinal inflammation 18, 19, 20, 21. ILC3s can rapidly respond to external stimuli and play critical roles in host defense, the resolution of inflammation and initiation of tissue repair in the gut 21, 22, 23, 24, 25, 26. These protective effects of ILC3s are mostly dependent on their production of the reparative cytokine IL‐22.…”

Section: Introductionmentioning

confidence: 99%

Purine metabolism controls innate lymphoid cell function and protects against intestinal injury

et al. 2018

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Inflammatory bowel disease (IBD) is a condition of chronic inflammatory intestinal disorder with increasing prevalence but limited effective therapies. The purine metabolic pathway is involved in various inflammatory processes including IBD. However, the mechanisms through which purine metabolism modulates IBD remain to be established. Here, we found that mucosal expression of genes involved in the purine metabolic pathway is altered in patients with active ulcerative colitis (UC), which is associated with elevated gene expression signatures of the group 3 innate lymphoid cell (ILC3)–interleukin (IL)‐22 pathway. In mice, blockade of ectonucleotidases (NTPDases), critical enzymes for purine metabolism by hydrolysis of extracellular adenosine 5′‐triphosphate (eATP) into adenosine, exacerbates dextran‐sulfate sodium‐induced intestinal injury. This exacerbation of colitis is associated with reduction of colonic IL‐22‐producing ILC3s, which afford essential protection against intestinal inflammation, and is rescued by exogenous IL‐22. Mechanistically, activation of ILC3s for IL‐22 production is reciprocally mediated by eATP and adenosine. These findings reveal that the NTPDase‐mediated balance between eATP and adenosine regulates ILC3 cell function to provide protection against intestinal injury and suggest potential therapeutic strategies for treating IBD by targeting the purine–ILC3 axis.

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“…As previously mentioned, DCs stimulated with MDP express high levels of IL-23 and IL-1β [64], cytokines that can induce production of IL-22 from RORγt + ILCs [111,112]. IL-22 has been reported to ameliorate intestinal inflammation in a murine model of experimental colitis [113], and bolster intestinal epithelial barrier function by upregulation of antimicrobial peptides [114]. Overall, additional studies are, however, required to clarify the MDP signaling and its influence on ILCs responses.…”

Section: Listeria Monocytogenes Citrobacter Rodentium Salomonella Amentioning

confidence: 99%

Muramyl dipeptide responsive pathways in Crohn’s disease: from NOD2 and beyond

Salem

Seidelin

Rogler

et al. 2012

Cell. Mol. Life Sci.

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Crohn's disease (CD) is one of main disease entities under the umbrella term chronic inflammatory bowel disease. The etiology of CD involves alterations in genetic, microbiological, and immunological factors. This review is devoted to the role of the bacterial wall compound muramyl dipeptide (MDP) for the activation of inflammatory pathways involved in the pathogenesis of CD. The importance of this molecule is underscored by the fact that (1) MDP, which is found in most Gram-negative and -positive bacteria, is able to trigger several immunological responses in the intestinal system, and (2) that alterations in several mediators of the MDP response including-but not restricted to-nucleotide oligomerization domain 2 (NOD2) are associated with CD. The normalization of MDP signaling is one of several important factors that influence the intestinal inflammatory response, a fact which emphasizes the pathogenic importance of MDP signaling for the pathogenesis of CD. The important aspects of NOD2 and non-NOD2 mediated effects of MDP for the development of CD are highlighted, as well as how alterations in these pathways might translate into the development of new therapeutic strategies.

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IL-22 ameliorates intestinal inflammation in a mouse model of ulcerative colitis

Abstract: Expression of IL-22 is induced in several human inflammatory conditions, including inflammatory bowel disease (IBD).

Cited by 709 publications

References 53 publications

Cytokines and effector T cell subsets causing autoimmune CNS disease

Cytokines and effector T cell subsets causing autoimmune CNS disease

Purine metabolism controls innate lymphoid cell function and protects against intestinal injury

Muramyl dipeptide responsive pathways in Crohn’s disease: from NOD2 and beyond

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