ArticlePloS one2013
Interleukin-17 expression positively correlates with disease severity of lupus nephritis by increasing anti-double-stranded DNA antibody production in a lupus model induced by activated lymphocyte derived DNA.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 43 citations in OpenAlex.
- Molecular consideration relevant to the mechanism of the comorbidity between psoriasis and systemic lupus erythematosus (Review).Experimental and therapeutic medicine · 2023Review
- Is Th17-Targeted Therapy Effective in Systemic Lupus Erythematosus?Current issues in molecular biology · 2023Review
- A Mechanistic Insight into the Pathogenic Role of Interleukin 17A in Systemic Autoimmune Diseases.Mediators of inflammation · 2022Review
- 5,6,7,8-Tetrahydrobenzo[4,5]thieno[2,3-d]pyrimidine derivative attenuates lupus nephritis with less effect to thymocyte development.Immunologic research · 2021Article
- The Th17/IL-17 Axis and Kidney Diseases, With Focus on Lupus Nephritis.Frontiers in medicine · 2021Review
- Lack of IL-17 Receptor A signaling aggravates lymphoproliferation in C57BL/6 lpr mice.Scientific reports · 2019Article
- Adaptive and Innate Immunity in Psoriasis and Other Inflammatory Disorders.Frontiers in immunology · 2019Review
- Administration of activated lymphocyte-derived DNA accelerates and aggravates lupus nephritis in B6/lpr mice: a new approach to modify a lupus murine model.Clinical and experimental immunology · 2018Article
- T cells and autoimmune kidney disease.Nature reviews. Nephrology · 2017Review
- JAK3-STAT pathway blocking benefits in experimental lupus nephritis.Arthritis research & therapy · 2016Article
- Current knowledge on psoriasis and autoimmune diseases.Psoriasis (Auckland, N.Z.) · 2016Review
- The Role of the Transcription Factor Ets1 in Lupus and Other Autoimmune Diseases.Critical reviews in immunology · 2016Article
- Signal transducer and activator of transcription (STAT) 3 inhibition delays the onset of lupus nephritis in MRL/lpr mice.Clinical immunology (Orlando, Fla.) · 2015Article
- HMGB1 Promotes Systemic Lupus Erythematosus by Enhancing Macrophage Inflammatory Response.Journal of immunology research · 2015Article
- Interleukin-6 promotes systemic lupus erythematosus progression with Treg suppression approach in a murine systemic lupus erythematosus model.Clinical rheumatology · 2014Article
- Endogenous interleukin (IL)-17A promotes pristane-induced systemic autoimmunity and lupus nephritis induced by pristane.Clinical and experimental immunology · 2014Article
- Anti-myelin antibodies play an important role in the susceptibility to develop proteolipid protein-induced experimental autoimmune encephalomyelitis.Clinical and experimental immunology · 2014Article
- Detection of dynamic frequencies of Th17 cells and their associations with clinical parameters in patients with systemic lupus erythematosus receiving standard therapy.Clinical rheumatology · 2014Article
- IL-17 in the rheumatologist's line of sight.BioMed research international · 2013Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Lupus nephritis is one of the most serious manifestations and one of the strongest predictors of a poor outcome in systemic lupus erythematosus (SLE). Recent evidence implicated a potential role of interlukin-17 (IL-17) in the pathogenesis of lupus nephritis. However, the correlation between IL-17 expression level and the severity of lupus nephritis still remains incompletely understood. In this study, we found that serum IL-17 expression level was associated with the severity of lupus nephritis, which was evaluated by histopathology of kidney sections and urine protein. Of note, we showed that enforced expression of IL-17 using adenovirus construct that expresses IL-17 could enhance the severity of lupus nephritis, while blockade of IL-17 using neutralizing antibody resulted in decreased severity of lupus nephritis. Consistently, we observed an impaired induction of lupus nephritis in IL-17-deficient mice. Further, we revealed that IL-17 expression level was associated with immune complex deposition and complement activation in kidney. Of interest, we found that IL-17 was crucial for increasing anti-double-stranded DNA (dsDNA) antibody production in SLE. Our results suggested that IL-17 expression level positively correlated with the severity of lupus nephritis, at least in part, because of its contribution to anti-dsDNA antibody production. These findings provided a novel mechanism for how IL-17 expression level correlated with disease pathogenesis and suggested that management of IL-17 expression level was a potential and promising approach for treatment of lupus nephritis.
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