IL-22BP

Last update 08 May 2025

Basic Info

Synonyms

CRF2-10, CRF2-S1, Cytokine receptor class-II member 10

+ [13]

Introduction

Isoform 2 is a receptor for IL22. Binds to IL22, prevents interaction with the functional IL-22R complex and blocks the activity of IL22 (in vitro). May play an important role as an IL22 antagonist in the regulation of inflammatory responses. Isoform 1 may play a role in establishing and maintaining successful pregnancy.

100 Clinical Results associated with IL-22BP

100 Translational Medicine associated with IL-22BP

0 Patents (Medical) associated with IL-22BP

159

Literatures (Medical) associated with IL-22BP

01 Apr 2025·International Immunopharmacology

Brusatol ameliorates intestinal mucosal injury in ulcerative colitis via activating IL-22/STAT3 pathway

Article

Author: Xie, Jianhui ; Wu, Minghui ; Lai, Zixuan ; Mai, Liting ; Su, Ziren ; Chen, Li ; Xu, Ying ; Chen, Jiannan ; Chen, Baoyi ; Lai, Zhengquan ; Xie, Youliang ; Hu, Xiaoxia ; Ai, Weipeng ; Liao, Huijun

Brusatol (BR) is an active compounds isolated from Brucea javanica, a Chinese herbal medicine that is famous for its anti-diarrheal effect. We have previously reported that BR mitigated inflammation in murine ulcerative colitis (UC) models. However, BR's role in intestinal mucosal healing, which is recently established as central strategy for the prevention and treatment of UC, remains unknown. In this study, the ameliorative effect of BR on intestinal mucosal damage was investigated in DSS-induced UC mice. BR significantly alleviated colitis symptoms, improved intestinal barrier function by preventing loss of goblet cells and downregulation of mucins and tight junction proteins, as well as maintained proliferative and apoptotic homeostasis in the colonic epithelium of UC mice. Mechanistically, BR enhanced the level and secretion of IL-22, but inhibited IL-22BP, an inhibitory protein of IL-22, in the blood serum and intestinal tissues of UC mice, as well as in MNK3 cells which is an effective cell model for studying ILC3s. Additionally, BR elevated the expressions of receptors for IL-22 (IL-10R2 and IL-22R1), and activated its downstream STAT3 signaling pathway. Furthermore, the involvement of IL-22 was further investigated by using recombinant IL-22 (rIL-22) and IL-22 antibody (anti-IL-22). BR demonstrated comparable effects with rIL-22 on alleviating intestinal inflammation and repairing intestinal mucosal injury. Treatment with anti-IL-22 abrogated the mucosal protective effects of BR. The present findings shed novel insights into the role of BR in intestinal mucosal healing via activating IL-22/STAT3 signaling pathway in UC.

01 Apr 2025·Cellular and Molecular Gastroenterology and Hepatology

IL-22BP modulates injury in acute pancreatitis but delays tissue recovery in chronic pancreatitis

Article

Author: Pasca Di Magliano, Marina ; McGue, Jake J ; Spiteri, Andrew G ; Zhang, Yaqing ; Frankel, Timothy L ; Griffith, Brian D ; Olivei, Alberto C ; Edwards, Jacob ; Sun, Lei

Interleukin-22 binding protein (IL-22BP) modulates IL-22 signaling impacting recovery following acute pancreatitis. However, in chronic pancreatitis deletion of IL-22BP results in persistent inflammation and fibrosis due to uncontrolled IL-22 activity leading to delayed tissue recovery.BACKGROUND & AIMSIn acute pancreatitis, IL-22 signaling is increased while overall expression of the cytokine paradoxically drops suggesting an additional level of control. Here, we investigate the regulation of IL-22 signaling by its soluble neutralizing receptor IL-22BP in the context of both acute and chronic pancreatitis.METHODSCerulein was used to induce acute and chronic pancreatitis in both wild-type mice and IL-22BP knockout mice. Histology, multiplex immunofluorescence (mIF) and flow cytometry were performed to compare differences in tissue injury, recovery, fibrosis, and inflammation at various times of recovery.RESULTSLoss of IL-22BP resulted in increased canonical IL-22 signaling and the expression of the anti-autophagy protein Bcl-XL. This was associated with decreased severity of acute pancreatitis as evidenced by lower serum amylase and tissue injury. In chronic pancreatitis, IL-22BP expression was induced in the inflammatory and recovery phases and genetic deletion resulted in unchecked IL-22 signaling, as demonstrated by persistent p-Stat3 signaling and proliferation of both epithelial cells and fibroblasts. Loss of IL-22BP increased myeloid cell infiltration which persisted throughout recovery. Mechanistically, IL-22 activity forced persistent acinar to ductal metaplasia and delayed tissue recovery.CONCLUSIONSIL-22BP plays an important role in modulating IL-22 activity during tissue injury and recovery after pancreatitis. Loss of IL-22BP attenuated acute pancreatitis but promoted chronic fibrosis and inflammation through uncontrolled IL-22 signaling and subsequent deleterious effects on epithelial cells, fibroblasts, and immune infiltration.

01 Feb 2025·Mucosal Immunology

RelB and C/EBPα critically regulate the development of Peyer’s patch mononuclear phagocytes

Article

Author: Kanaya, Takashi ; Tachibana, Naoko ; Kato, Tamotsu ; Shiroguchi, Katsuyuki ; Ohno, Hiroshi ; Jinnohara, Toshi ; Riemann, Marc ; Kawakami, Eiryo ; Sakakibara, Sayuri ; Jin, Jianshi ; Sasaki, Takaharu

To establish protection against harmful foreign antigens, the small intestine harbors guardian sites called Peyer's patches (PPs). PPs take up antigens through microfold (M) cells and transfer them to the sub-epithelial dome (SED), which contains a high density of mononuclear phagocytes (MPs), for T cell-priming. Accumulating evidence indicates that SED-MPs have unique functions other than T cell-priming to facilitate mucosal immune responses; however, the crucial factors regulating the functions of SED-MPs have not been determined. Here we performed transcriptome analysis, and identified the gene signatures of SED-MPs. Further data interpretation with transcription factor (TF) enrichment analysis estimated TFs responsible for the functions of SED-MPs. Among them, we found that RelB and C/EBPα were preferentially activated in SED-MPs. RelB-deficiency silenced the expression of IL-22BP and S100A4 by SED-MPs. On the other hand, C/EBPα-deficiency decreased the expression of lysozyme by SED-MPs, resulting the increased invasion of orally administered pathogenic bacteria into PPs and mesenteric lymph nodes. Our findings thus demonstrate that RelB and C/EBPα are essential to regulate the functions of SED-MPs.

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IL-22BP

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