ArticleClinical and translational medicine2021
A novel potential target of IL-35-regulated JAK/STAT signaling pathway in lupus nephritis.
Article in Clinical and translational medicine, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 37 citations in OpenAlex.
- IL-35 promotes synovial fibroblast senescence via activation of cGAS-STING-TBK1-IRF3 pathway in rheumatoid arthritis.Immunity & ageing : I & A · 2026Article
- Circulating long non-coding RNAs as diagnostic markers of lupus nephritis and 5-year follow-up disease flares.Frontiers in immunology · 2026Article
- Hyperoside Attenuates Lupus Nephritis-Associated Mesangial Cell Apoptosis via the P53/XAF1 Pathway: Integrative Bioinformatics and In Vitro Validation.Journal of inflammation research · 2026Article
- Inflammatory drivers of carotid atherosclerosis: signaling pathways, immune cells, and plaque stability.Frontiers in cardiovascular medicine · 2026Review
- Lidocaine Modulates Cytokine Production and Reprograms the Tumor Immune Microenvironment to Enhance Anti-Tumor Immune Responses in Gastric Cancer.International journal of molecular sciences · 2025Article
- Mechanisms and therapeutic prospect of the JAK-STAT signaling pathway in liver cancer.Molecular and cellular biochemistry · 2025Review
- Inflammation in glomerular diseases.Frontiers in immunology · 2025Review
- T-Cell Phenotypes and Systemic Cytokine Profiles of People Living with HIV Admitted to Hospital with COVID-19.Microorganisms · 2024Article
- Noninvasive biomarkers for lupus nephritis.Laboratory medicine · 2024Review
- Assay for interferon gamma release as a novel marker in pediatric patients with systemic lupus erythematosus.Pediatric rheumatology online journal · 2024Article
- TREM2 deficiency aggravates renal injury by promoting macrophage apoptosis and polarization via the JAK-STAT pathway in mice.Cell death & disease · 2024Article
- The oncogenic mechanisms of the Janus kinase-signal transducer and activator of transcription pathway in digestive tract tumors.Cell communication and signaling : CCS · 2024Review
- Role and mechanism of esketamine in improving postoperative cognitive dysfunction in aged mice through the TLR4/MyD88/p38 MAPK pathway.The Kaohsiung journal of medical sciences · 2024Article
- Reprogramming of regulatory T cells in inflammatory tumor microenvironment: can it become immunotherapy turning point?Frontiers in immunology · 2024Review
- The Inflammatory and Oxidative Status of Newly Diagnosed Class III and Class IV Lupus Nephritis, with Six-Month Follow-Up.Antioxidants (Basel, Switzerland) · 2023Article
- Immune interactions in pembrolizumab (PD-1 inhibitor) cancer therapy and cardiovascular complications.American journal of physiology. Heart and circulatory physiology · 2023Review
- AZGP1 as a potential biomarker of IgA vasculitis with nephritis in a children‑based urinary proteomics study by diaPASEF.Molecular medicine reports · 2023Article
- Decipher the Immunopathological Mechanisms and Set Up Potential Therapeutic Strategies for Patients with Lupus Nephritis.International journal of molecular sciences · 2023Review
- Diabetic complications and prospective immunotherapy.Frontiers in immunology · 2023Review
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Authors and funding
10 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn this study, we have investigated the potential regulatory mechanisms of IL-35 to relieve lupus nephritis (LN) through regulating Janus kinase (JAK)/signal transducers and activators of transcription (STAT) signaling pathway in mesangial cells.
resultsAmong 105 significant differentially expressed proteins (DEPs) between juvenile systemic lupus erythematosus (JSLE) patients with LN and healthy controls, LAIR1, PDGFRβ, VTN, EPHB4, and EPHA4 were downregulated in JSLE-LN. They consist of an interactive network with PTPN11 and FN1, which involved in IL-35-related JAK/STAT signaling pathway. Besides, urinary LAIR1 was significantly correlated with JSLE-LN clinical parameters such as SLEDAI-2K, %CD19+ B, and %CD3+ T cells. Through bioinformatics analysis of co-immunoprecipitation with mass spectrometry results, including GO, KEGG, and STRING, five genes interacted with Lair1 were upregulated by IL-35, but only Myh10 was downregulated. Therefore, we presumed an interactive network among these DEPs, JAK/STAT, and IL-35. Moreover, the downregulated phosphorylated (p)-STAT3, p-p38 MAPK, and p-ERK, and the upregulated p-JAK2/p-STAT1/4 in IL-35 overexpressed mesangial cells, and RNA-sequencing results validated the potential regulatory mechanisms of IL-35 in alleviating JSLE-LN disease. Moreover, the relieved histopathological features of nephritis including urine protein and leukocyte scores, a decreased %CD90
conclusionsOur study provided a reference proteomic map of urinary biomarkers for JSLE-LN and elucidated evidence that IL-35 may regulate the interactive network of LAIR1-PTPN11-JAK-STAT-FN1 to affect JAK/STAT and MAPK signaling pathways to alleviate inflammation in JSLE-LN. This finding may provide a further prospective mechanism for JSLE-LN clinical treatment.
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