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Last update 08 May 2025

IL-10Rα

Last update 08 May 2025

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

WO2022150788

Patent Mining

Target

IL-10Rα

Mechanism-

Active Org.

Synthekine, Inc.

Originator Org.

Synthekine, Inc.

Active Indication

Endocrinology and Metabolic Disease [+7]

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

514

Literatures (Medical) associated with IL-10Rα

01 May 2025·World Neurosurgery

Causal Association Between Inflammatory Proteins, Inflammatory Cells, and Cauda Equina Syndrome: A Two-Sample Mendelian Randomization

Article

Author: Sun, Kaiqiang ; Sun, Xiaofei ; Shi, Jiangang ; Han, Linhui ; Wang, Yuan ; Xing, Jianpeng ; Zhang, Bin ; Kong, Qingjie ; Wang, Jinyu

BACKGROUNDRecent studies have shown that inflammation plays a crucial role in the progression of cauda equina syndrome (CES). However, the exact cause-and-effect relationship between them is still unclear.METHODSWe used CES data from the FinnGen genome-wide association study (GWAS), containing 329 cases and 408,351 control patients. Inflammatory proteins data were obtained from a large scale GWAS of 14,828 European ancestry participants, and inflammatory cells data were obtained from a GWAS summary of 3757 Sardinians. We chose inverse variance weighted as the main method and the Cochrane Q test to assess heterogeneity in the results. The MR-Egger intercept test and MR pleiotropy residual sum and outliers test were used to evaluate the horizontal pleiotropy, and sensitivity analysis was performed by leave-one-out analysis.RESULTSWe examined robust associations between inflammatory proteins, inflammatory cells, and CES using Mendelian randomization. Two inflammatory proteins and 12 inflammatory cells were found as risk factors for CES: IL-8 and PD-L1; and basophil plasmacytoid dendritic cell, CD86+plasmacytoid dendritic cell, CD62L-plasmacytoid dendritic cell, CD39+secreting Treg, IgD+CD38-B cell, switched memory B cell, IgD+CD24+B cell, CD62L+dendritic cell, CD4+T cell, γδ T cell, and CD33dim HLA DR-myeloid cell. Two inflammatory proteins and 7 inflammatory cells were found as protective factors for CES: IL-10RA and CCL25; and transitional B cell, terminal differentiation double negative T cell, CD28-CD127-CD25++CD8br T cell, IgD+CD38br B cell, CD28+CD45RA-CD8br Treg, IgD+CD38-naive B cell, and granulocyte. Heterogeneity and pleiotropy analysis confirmed the reliability of the results. Our study reveals the causal relationship between inflammatory proteins, inflammatory cells, and CES, offering new insights for the development of future therapeutic drugs and early warning indicators.CONCLUSIONSOur findings extend genetic research to causal analysis between inflammatory proteins, cells, and CES. We found 2 proteins and 12 cells as risk factors and 2 proteins and 7 cells as protective factors. Further investigations are needed to verify whether these inflammation markers can be used to prevent or treat CES.

01 Mar 2025·International Immunopharmacology

The novel role of LCK and other PcDEGs in the diagnosis and prognosis of sepsis: Insights from bioinformatic identification and experimental validation

Article

Author: Kong, Fanyu ; Yang, Min ; Liu, Xiandong ; Tang, Lunxian ; Ling, Bingrui ; Zhou, Xiaohui ; Xu, Jiani ; Chen, Kun ; Shao, Li ; Zhu, Yuxin ; Ji, Jinlu ; Wang, Chunxue ; Yang, Qian

BACKGROUNDProgrammed cell death (PCD) has emerged as a pivotal progress in pathogenesis of sepsis, but its role in identification of sepsis has not been fully understood.METHODSDifferentially expressed genes (DEGs) were identified from the GEO database. PCD-related genes were intersected with DEGs, and key PcDEGs were identified through the protein-protein interaction (PPI) network. To pinpoint hub PcDEGs in sepsis, we applied Random Forest (RF), Support Vector Machine (SVM), Extreme Gradient Boosting (XGB), and Generalized Linear Model (GLM) algorithms. Additionally, the expression levels of five hub PcDEGs were validated in single cell RNA sequencing of sepsis patients and peripheral blood mononuclear cells (PBMCs) from a clinical cohort by quantitative real-time PCR (qRT-PCR). LCK expression was further determined by ELISA, and its diagnostic and prognostic value was evaluated using ROC analysis. LCK levels in the cecal ligation and puncture (CLP)-induced sepsis mouse model were assessed by Western blot and Immunofluorescence (IF). Finally, we assessed the regulatory role of LCK in cell apoptosis using flow cytometry and Western blot analysis.RESULTS70 PcDEGs were identified by intersecting 690 DEGs and 1254 PCD-related genes. PPI analysis identified top 15 genes based on Degree algorithm. We then identified five hub PcDEGs (LCK, IL10RA, CD3E, CD5 and ITGAM) that could serve as biomarkers through machine learning. As the expressions of LCK, IL10RA, CD3E and CD5 decreased and ITGAM expression was upregulated in septic patients. Consistently, Serum LCK concentration was reduced in septic patients, and the area under the ROC curve (AUC) of LCK was 0.753. Importantly, LCK displayed more pronounced reduction in non-survivors and those with septic shock than survivors and non-shock patients. The AUC for LCK was 0.726 in predicting mortality of septic patients. Moreover, we observed a decrease expression of LCK in the vital organs (liver, lung, spleen, thymus and PBMC) of septic mice model which mirrored observations in septic patients. Finally, we found that inhibiting LCK promoted apoptosis in Jurkat cells.CONCLUSIONSOur study reveals that PcDEGs are dysregulated in sepsis, and closely related to disease pathology. Our finding provides new insights into clinical identification and outcome prediction of sepsis. Of note, LCK is a new biomarker for diagnosis and prognosis, which might be a potential therapeutic target for the treatment of sepsis.

01 Mar 2025·Pulmonary Pharmacology & Therapeutics

IL-10RA promotes lung cancer cell proliferation by increasing fatty acid oxidation via STAT3 signaling pathway

Article

Author: Feng, Xiaofan ; Li, Xueying ; Deng, Weimin ; Zhang, Haoke ; Liu, Zihe ; Chen, Siqi ; Wang, Bo ; Yu, Chunyan ; Liu, Zixuan ; Ouyang, Yuqing ; Du, Wei

Metabolic reprogramming in tumor cells plays a crucial role in promoting cell proliferation and metastasis, and is currently recognized as a significant marker of tumor progression. Interleukin-10 receptor subunit alpha (IL-10RA), a member of the type II cytokine receptor family, is predominantly expressed on macrophages and T cells and plays a crucial role in regulating immune cell metabolism and immune response. However, its role in the energy metabolic pathways of tumor cells remains unclear. In this study, we found increased expression of IL-10RA in human non-small cell lung cancer (NSCLC), and a correlation between increased IL-10RA expression and tumor stage, tumor size, and short overall survival of patients with NSCLC. IL-10RA overexpression significantly promoted the proliferation of NSCLC cell lines and enhanced glycolysis and fatty acid oxidation (FAO), thereby boosting energy production. Correspondingly, the downregulation of IL-10RA inhibited proliferation, glycolysis, and FAO in NSCLC cell lines. Bioinformatic analyses indicated that IL-10RA upregulates the signal transducer and activator of transcription 3 (STAT3) signaling pathway. STAT3 inhibitor effectively blocked the increase in FAO levels and cell proliferation induced by IL-10RA overexpression. These findings suggest that IL-10RA accelerates NSCLC cell proliferation by increasing FAO levels via the STAT3 pathway, highlighting IL-10RA as a potential therapeutic target for NSCLC.

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IL-10Rα

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