ArticleRheumatology (Oxford, England)2021
Splicing factor SRSF1 limits IFN-γ production via RhoH and ameliorates experimental nephritis.
Article in Rheumatology (Oxford, England), 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 24 citations in OpenAlex.
- Application of the nephrotoxic serum nephritis model in glomerulonephritis research.Molecular medicine (Cambridge, Mass.) · 2026Review
- Immune dysfunction in Alzheimer disease.Nature reviews. Neuroscience · 2026Review
- Exosomal miR-2110 from PM2.5-Exposed Lung Epithelial Cells Targets SRSF1 to Promote M1 Macrophage Polarization and Inflammatory Responses in COPD.International journal of chronic obstructive pulmonary disease · 2026Article
- miR-7974 as a potential biomarker for lupus nephritis and its involvement in disease progression.BMC nephrology · 2025Article
- Uncovering protein prenylation in Th1 cells: novel prenylation sites and insights into statin and farnesyltransferase inhibition.BMC biology · 2025Article
- Identification of serum exosomal miRNA biomarkers in patients with lupus nephritis.Clinical rheumatology · 2025Article
- Review
- Serine and arginine rich splicing factor 1: a potential target for neuroprotection and other diseases.Neural regeneration research · 2023Review
- Emerging roles of spliceosome in cancer and immunity.Protein & cell · 2022Review
- 2-Arachidonoylglycerol Reduces the Production of Interferon-Gamma in T Lymphocytes from Patients with Systemic Lupus Erythematosus.Biomedicines · 2022Article
- Nuclear speckle integrity and function require TAO2 kinase.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- RNA-binding proteins and their role in kidney disease.Nature reviews. Nephrology · 2022Review
- Splicing factor SRSF1 controls distinct molecular programs in regulatory and effector T cells implicated in systemic autoimmune disease.Molecular immunology · 2022Article
- IFN-γ promotes the development of systemic lupus erythematosus through the IFNGR1/2-PSTAT1-TBX21 signaling axis.American journal of translational research · 2022Article
- Review
- Tim-1 alleviates lupus nephritis-induced podocyte injury via regulating autophagy.Central-European journal of immunology · 2021Article
- Estradiol in Systemic Lupus Erythematosus.Acta endocrinologica (Bucharest, Romania : 2005)Article
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5 authors at 1 institution in 1 country.
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Abstract
objectiveCD4 T helper 1 (Th1) cells producing IFN-γ contribute to inflammatory responses in the pathogenesis of SLE and lupus nephritis. Moreover, elevated serum type II IFN levels precede the appearance of type I IFNs and autoantibodies in patient years before clinical diagnosis. However, the molecules and mechanisms that control this inflammatory response in SLE remain unclear. Serine/arginine-rich splicing factor 1 (SRSF1) is decreased in T cells from SLE patients, and restrains T cell hyperactivity and systemic autoimmunity. Our objective here was to evaluate the role of SRSF1 in IFN-γ production, Th1 differentiation and experimental nephritis.
methodsT cell-conditional Srsf1-knockout mice were used to study nephrotoxic serum-induced nephritis and evaluate IFN-γ production and Th1 differentiation by flow cytometry. RNA sequencing was used to assess transcriptomics profiles. RhoH was silenced by siRNA transfections in human T cells by electroporation. RhoH and SRSF1 protein levels were assessed by immunoblots.
resultsDeletion of Srsf1 in T cells led to increased Th1 differentiation and exacerbated nephrotoxic serum nephritis. The expression levels of RhoH are decreased in Srsf1-deficient T cells, and silencing RhoH in human T cells leads to increased production of IFN-γ. Furthermore, RhoH expression was decreased and directly correlated with SRSF1 in T cells from SLE patients.
conclusionOur study uncovers a previously unrecognized role of SRSF1 in restraining IFN-γ production and Th1 differentiation through the control of RhoH. Reduced expression of SRSF1 may contribute to pathogenesis of autoimmune-related nephritis through these molecular mechanisms.
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