Last update 01 Nov 2024

IL-10Rα

Last update 01 Nov 2024

Basic Info

Synonyms

CD210, CD210a, CDw210a

+ [12]

Introduction

Cell surface receptor for the cytokine IL10 that participates in IL10-mediated anti-inflammatory functions, limiting excessive tissue disruption caused by inflammation. Upon binding to IL10, induces a conformational change in IL10RB, allowing IL10RB to bind IL10 as well (PubMed:16982608). In turn, the heterotetrameric assembly complex, composed of two subunits of IL10RA and IL10RB, activates the kinases JAK1 and TYK2 that are constitutively associated with IL10RA and IL10RB respectively (PubMed:12133952). These kinases then phosphorylate specific tyrosine residues in the intracellular domain in IL10RA leading to the recruitment and subsequent phosphorylation of STAT3. Once phosphorylated, STAT3 homodimerizes, translocates to the nucleus and activates the expression of anti-inflammatory genes. In addition, IL10RA-mediated activation of STAT3 inhibits starvation-induced autophagy (PubMed:26962683).

Drugs associated with IL-10Rα

WO2022031885

Patent Mining

Target

IL-10Rα

Mechanism-

Active Org.

Synthekine, Inc.Startup

Originator Org.

Synthekine, Inc.Startup

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

WO2022150788

Patent Mining

Target

IL-10Rα

Mechanism-

Active Org.

Synthekine, Inc.Startup

Originator Org.

Synthekine, Inc.Startup

Active Indication

Infectious Diseases

Inactive Indication-

Drug Highest PhaseDiscovery

First Approval Ctry. / Loc.-

First Approval Date20 Jan 1800

100 Clinical Results associated with IL-10Rα

100 Translational Medicine associated with IL-10Rα

0 Patents (Medical) associated with IL-10Rα

549

Literatures (Medical) associated with IL-10Rα

31 Dec 2024·Renal Failure

Identification of common and specific fibrosis-related genes in three common chronic kidney diseases

Article

Author: Sun, Guannan ; Liu, Chao ; Dong, Zheyi ; Geng, Xiaodong ; Cai, Guangyan ; Chen, Xiangmei ; Hong, Quan ; Shen, Wanjun ; Fu, Zhangning

BACKGROUNDKidney fibrosis is the common final pathway of virtually all advanced forms of chronic kidney disease (CKD) including diabetic nephropathy (DN), IgA nephropathy (IgAN) and membranous nephropathy (MN), with complex mechanism. Comparative gene expression analysis among these types of CKD may shed light on its pathogenesis. Therefore, we conducted this study aiming at exploring the common and specific fibrosis-related genes involved in different types of CKD.METHODSKidney biopsy specimens from patients with different types of CKD and normal control subjects were analyzed using the NanoString nCounter® Human Fibrosis V2 Panel. Genes differentially expressed in all fibrotic DN, IgAN and MN tissues compared to the normal controls were regarded as the common fibrosis-related genes in CKD, whereas genes exclusively differentially expressed in fibrotic DN, IgAN or MN samples were considered to be the specific genes related to fibrosis in DN, IgAN and MN respectively. Quantitative real-time PCR (qRT-PCR) was performed to validate the expression of the selected genes.RESULTSProtein tyrosine phosphatase receptor type C (PTPRC), intercellular cell adhesion molecule-1 (ICAM1), vascular cell adhesion molecule-1 (VCAM1), interleukin 10 receptor alpha (IL10RA) and CC chemokine receptor 2 (CCR2) were identified as the potential common genes for kidney fibrosis in different types of CKD, while peroxisome proliferator-activated receptor alpha (PPARA), lactate oxidase (LOX), secreted phosphoprotein 1 (SPP1) were identified as the specific fibrosis-associated genes for DN, IgAN and MN respectively. qRT-PCR demonstrated that the expression levels of these selected genes were consistent with the NanoString analysis.CONCLUSIONSThere were both commonalities and differences in the mechanisms of fibrosis in different types of CKD, the commonalities might be used as the common therapeutic targets for kidney fibrosis in CKD, while the differences might be used as the diagnostic markers for DN, IgAN and MN respectively. Inflammation was highly relevant to the pathogenesis of fibrosis. This study provides further insight into the pathophysiology and treatment of fibrotic kidney disease.

01 Dec 2024·Cytokine

Neutrophil-derived IL-10 increases CVB3-induced acute pancreatitis pathology via suppressing CD8+T cell activation while increasing macrophage STAT3-IL-6 cascade

Article

Author: Sun, Zhirong ; Yang, Yue ; Li, Jingrou ; Song, Yahui ; Xu, Wei

Acute pancreatitis (AP) is a lethal inflammatory disease of the pancreas. Its pathogenesis remains obscure and specific treatments are lacking. An increase in Interleukin-10 (IL-10) in the early stage of AP patients is closely related to AP severity. In Coxsackievirus B3 (CVB3) induced murine AP model, we found early IL-10 increased viral replication and pancreatic inflammation, yet the cellular source of IL-10 and the immunomodulatory role of neutrophils during viral infection remains unknown. Here we show that CVB3 infection enhanced neutrophil infiltration and IL-10 expression in the pancreas at day3 post infection (p.i.). Neutrophils served as an important early source of pancreatic IL-10 at the initiation of infection. Day3 pancreas extracts (D3P) also induced bone-marrow derived neutrophils (BMneu) to secrete IL-10. Adoptive transfer of D3P-pretreated BMneu into IL-10 KO mice increased viral replication and pancreas histopathology, which effect was blunted by the absence of IL-10 in BMneu. Mechanically, IL-10⁺ neutrophil increased IL-10R1 expression on MΦs and activated STAT3-IL-6/IL-10 signaling cascade while decreased IL-12 and MHC II expression in MΦs, thus impairing IFN-γ⁺Granzyme B⁺CD8⁺T cell activation and viral clearance. Adoptive transferring infected mice with activated CD8⁺T cells 4 days p.i. attenuated viral load and AP pathology indicating an AP-protective effect. Our findings document a novel immunoregulatory function of neutrophils in acute CVB3 infection, in which neutrophil-derived IL-10 impairs anti-viral CD8⁺T activation, and amplifies intrapancreatic inflammation via activating MΦ STAT3-IL-6 signaling cascade. An IL-10-targeting option is suggested for the future treatment of viral AP.

01 Oct 2024·Fish & Shellfish Immunology

Short time-series expression transcriptome data reveal the gene expression patterns and potential biomarkers of blood infection with LPS and poly (I:C) in Mandarin fish (Siniperca chuatsi)

Article

Author: Chen, Xiaowu ; Chen, Tiantian ; Aly, Rahma Sakina Said ; Jiang, Hewei ; Shen, Yawei ; Wang, Yongxiang ; Liu, Yufei

Blood transcriptomics has emerged as a vital tool for tracking the immune system and supporting disease diagnosis, prognosis, treatment, and research. The present study was conducted to analyze the gene expression profile and potential biomarker candidates using the whole blood of mandarin fish (Siniperca chuatsi) infected with LPS or poly (I:C) at 0 h, 3 h, 6 h, and 12 h. Our data suggest that 310 shared differentially expressed genes (DEGs) were identified among each comparison group after LPS infection, and 137 shared DEGs were identified after poly (I:C) infection. A total of 62 shared DEGs were differentially expressed in all compared groups after LPS or poly (I:C) infection. Pathways analysis for DEGs in all different compared groups showed that cytokine-cytokine receptor interaction was the most enrichment pathway. The expression levels of genes C-X-C chemokine receptor type 2-like (cxcr2), chemokine (C-C motif) receptor 9a (ccr9a), chemokine (C-C motif) receptor 9b (ccr9b), chemokine (C-X-C motif) receptor 4b (cxcr4b), and interleukin 10 receptor alpha (il10ra) were significantly different in all compared groups and most enriched in cytokine-cytokine receptor interaction pathway. The protein-protein interactions analysis among all shared DEGs showed that cxcr4 was the hub gene with the highest degree. The biomarker candidates discovered in this study may, following validation, prove effective as diagnostic tools in monitoring mandarin fish diseases.

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IL-10Rα

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