ArticleKidney diseases (Basel, Switzerland)2020
Leukemia Inhibitory Factor Signaling Enhances Production of Galactose-Deficient IgA1 in IgA Nephropathy.
Article in Kidney diseases (Basel, Switzerland), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 41 citations in OpenAlex.
- Development of IgA nephropathy following risankizumab therapy for psoriatic arthritis: a case report.CEN case reports · 2026Article
- Inhibition of p65 NF-κB enhances production of galactose-deficient IgA1 through suppression ofbioRxiv : the preprint server for biology · 2026Article
- Aberrant signaling in tonsillar B cells producing pathogenicFrontiers in immunology · 2026Review
- Dioscin attenuates Gd-IgA1 overproduction by inhibiting the IL-6-JAK2/STAT3 signaling axis in IgA nephropathy.BMC nephrology · 2025Article
- LncRNAs and IgA nephropathy: underlying molecular pathways and clinical applications.Clinical and experimental medicine · 2025Review
- Exploring the mediating role of immune cells in the pathogenesis of IgA nephropathy through the inflammatory axis of gut microbiota from a genomic perspective.Mammalian genome : official journal of the International Mammalian Genome Society · 2025Article
- The pathogenesis of IgA nephropathy and implications for treatment.Nature reviews. Nephrology · 2025Review
- Exploring the Relationship Between 91 Inflammatory Cytokines and IgA Nephropathy Using a Two-Sample Mendelian Randomization Study and the Gene Expression Omnibus Database.Mediators of inflammation · 2025Article
- The evolving understanding of systemic mechanisms in organ-specific IgA nephropathy: a focus on gut-kidney crosstalk.Theranostics · 2025Review
- Pathogenesis of IgA nephropathy: Omics data inform glycomedicine.Nephrology (Carlton, Vic.) · 2024Article
- Emerging Biochemical and Immunologic Mechanisms in the Pathogenesis of IgA Nephropathy.Seminars in nephrology · 2024Review
- IgA Nephropathy: Significance of IgA1-Containing Immune Complexes in Clinical Settings.Journal of clinical medicine · 2024Review
- LIF/JAK2/STAT1 Signaling Enhances Production of Galactose-Deficient IgA1 by IgA1-Producing Cell Lines Derived From Tonsils of Patients With IgA Nephropathy.Kidney international reports · 2024Article
- Review
- GWAS-follow-up Studies Identified a Connection between Abnormal LIF/JAK2/STAT1 Signaling and Overproduction of Galactose-Deficient IgA1 in the Tonsillar IgA1-Secreting Cells from Patients with IgA Nephropathy.Journal of clinical research & bioethics · 2024Article
- An Update on the Genetics of IgA Nephropathy.Journal of clinical medicine · 2023Review
- [Research advances in the etiology and pathogenesis of immunoglobulin A vasculitis].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2023Review
- Genome-wide association analyses define pathogenic signaling pathways and prioritize drug targets for IgA nephropathy.Nature genetics · 2023Article
- Racial heterogeneity of IgA1 hinge-regioniScience · 2022Article
- Phosphatase control of cytokine-mediated overproduction of galactose-deficient IgA1, the main autoantigen in IgA nephropathy.Journal of autoimmunity · 2022Article
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
objectivesIgA nephropathy (IgAN) is thought to involve an autoimmune process wherein galactose-deficient IgA1 (Gd-IgA1), recognized as autoantigen by autoantibodies, forms pathogenic immune complexes. Mounting evidence has implicated abnormal activation of some protein-tyrosine kinases (PTKs) in IgAN. Furthermore, genome-wide association studies (GWAS) of IgAN provided insight into disease pathobiology and genetics. A GWAS locus on chromosome 22q12 contains genes encoding leukemia inhibitory factor (LIF) and oncostatin M, interleukin (IL)-6-related cytokines implicated in mucosal immunity and inflammation. We have previously shown that IL-6 mediates overproduction of Gd-IgA1 through aberrant STAT3 activation. Here, we show that LIF enhanced production of Gd-IgA1 in IgA1-secreting cells of patients with IgAN and provide initial analyses of LIF signaling.
methodsWe characterized LIF signaling that is involved in the overproduction of Gd-IgA1, using IgA1-secreting cell lines derived from peripheral blood of patients with IgAN and healthy controls (HC). We used global PTK activity profiling, immunoblotting, lectin ELISA, and siRNA knock-down.
resultsLIF stimulation did not significantly affect production of total IgA1 in IgA1-secreting cells from patients with IgAN or HC. However, LIF increased production of Gd-IgA1, but only in the cells from patients with IgAN. LIF stimulation enhanced phosphorylation of STAT1 in IgA1-secreting cells from patients with IgAN to a higher degree than in the cells from HC. siRNA knock-down of STAT1 blocked LIF-mediated overproduction of Gd-IgA1. Unexpectedly, this abnormal phosphorylation of STAT1 in IgA1-secreting cells from patients with IgAN was not mediated by JAK, but rather involved activation of Src-family PTKs (SFKs).
conclusionAbnormal LIF/STAT1 signaling represents another pathway potentially leading to overproduction of Gd-IgA1 in IgAN, providing possible explanation for the phenotype associated with chromosome 22q12 GWAS locus. Abnormal LIF/STAT1 signaling and the associated SFKs may represent potential diagnostic and/or therapeutic targets in IgAN.
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