IL-22 promotes mucin-type O-glycosylation and MATH1+ cell-mediated amelioration of intestinal inflammation

Singh, Ankita; Beaupre, Michael; Villegas-Novoa, Cecilia; Shiomitsu, Kiyoshi; Gaudino, Stephen J.; Tawch, Suzanne; Damle, Ruhee; Kempen, Cody; Choudhury, Biswa; McAleer, Jeremy P.; Sheridan, Brian S.; Denoya, Paula; Blumberg, Richard S.; Hearing, Patrick; Allbritton, Nancy L.; Kumar, Pawan

doi:10.1016/j.celrep.2024.114206

Cell Reports

2024

DOI: 10.1016/j.celrep.2024.114206

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IL-22 promotes mucin-type O-glycosylation and MATH1+ cell-mediated amelioration of intestinal inflammation

Ankita Singh,

Michael Beaupre,

Cecilia Villegas-Novoa

et al.

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2024

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Cited by 3 publications

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Transcriptome analysis reveals modulations in glycosylation profiles of the mucosal barrier and their potential interaction with gut microbiota in weaned piglets

Cheng,

Li,

Zhao

et al. 2024

Animal Nutrition

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Transcriptome analysis reveals modulations in glycosylation profiles of the mucosal barrier and their potential interaction with gut microbiota in weaned piglets

Cheng,

Li,

Zhao

et al. 2024

Animal Nutrition

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Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells

Ohara,

Takeuchi,

Hirota

2024

Cell Mol Immunol

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The IL-23 signaling pathway in both innate and adaptive immune cells is vital for orchestrating type 17 immunity, which is marked by the secretion of signature cytokines such as IL-17, IL-22, and GM-CSF. These proinflammatory mediators play indispensable roles in maintaining intestinal immune equilibrium and mucosal host defense; however, their involvement has also been implicated in the pathogenesis of chronic inflammatory disorders, such as inflammatory bowel diseases and autoimmunity. However, the implications of type 17 immunity across diverse inflammation models are complex. This review provides a comprehensive overview of the multifaceted roles of these cytokines in maintaining gut homeostasis and in perturbing gut barrier integrity, leading to acute and chronic inflammation in various models of gut infection and colitis. Additionally, this review focuses on type 17 immunity interconnecting multiple organs in autoimmune conditions, with a particular emphasis on the pathogenesis of autoimmune arthritis and neuroinflammation driven by T cells primed within the gut microenvironment.

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Involvement of Intestinal Epithelium Aryl Hydrocarbon Receptor Expression and 3, 3′-Diindolylmethane in Colonic Tertiary Lymphoid Tissue Formation

Garcia-Villatoro,

Bomstein,

Allred

et al. 2024

IJMS

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Tertiary lymphoid tissues (TLTs) are adaptive immune structures that develop during chronic inflammation and may worsen or lessen disease outcomes in a context-specific manner. Immune cell activity governing TLT formation in the intestines is dependent on immune cell aryl hydrocarbon receptor (AhR) activation. Homeostatic immune cell activity in the intestines is further dependent on ligand activation of AhR in intestinal epithelial cells (IECs), yet whether AhR activation and signaling in IECs influences the formation of TLTs in the presence of dietary AhR ligands is not known. To this end, we used IEC-specific AhR deletion coupled with a mouse model of dextran sodium sulfate (DSS)-induced colitis to understand how dietary AhR ligand 3, 3′-diindolylmethane (DIM) influenced TLT formation. DIM consumption increased the size of TLTs and decreased T-cell aggregation to TLT sites in an IEC-specific manner. In DSS-exposed female mice, DIM consumption increased the expression of genes implicated in TLT formation (Interleukin-22, Il-22; CXC motif chemokine ligand 13, CXCL13) in an IEC AhR-specific manner. Conversely, in female mice without DSS exposure, DIM significantly reduced the expression of Il-22 or CXCL13 in iAhRKO mice, but this effect was not observed in WT animals. Our findings suggest that DIM affects the immunological landscape of TLT formation during DSS-induced colitis in a manner contingent on AhR expression in IECs and biological sex. Further investigations into specific immune cell activity, IEC-specific AhR signaling pathways, and dietary AhR ligand-mediated effects on TLT formation are warranted.

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IL-22 promotes mucin-type O-glycosylation and MATH1+ cell-mediated amelioration of intestinal inflammation

Cited by 3 publications

References 55 publications

Transcriptome analysis reveals modulations in glycosylation profiles of the mucosal barrier and their potential interaction with gut microbiota in weaned piglets

Transcriptome analysis reveals modulations in glycosylation profiles of the mucosal barrier and their potential interaction with gut microbiota in weaned piglets

Type 17 immunity: novel insights into intestinal homeostasis and autoimmune pathogenesis driven by gut-primed T cells

Involvement of Intestinal Epithelium Aryl Hydrocarbon Receptor Expression and 3, 3′-Diindolylmethane in Colonic Tertiary Lymphoid Tissue Formation

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