ArticleThe American journal of pathology1994
Interleukin-6 exacerbates glomerulonephritis in (NZB x NZW)F1 mice.
Article in The American journal of pathology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
51 citing papers in PubMed, 136 citations in OpenAlex.
- Lymphocytes Change Their Phenotype and Function in Systemic Lupus Erythematosus and Lupus Nephritis.International journal of molecular sciences · 2024Review
- Anti-complement factor H (CFH) autoantibodies could delay pristane-induced lupus nephritis.Immunologic research · 2023Article
- Effects of high fat diet-induced obesity on pathophysiology, immune cells, and therapeutic efficacy in systemic lupus erythematosus.Scientific reports · 2022Article
- B Cell Aberrance in Lupus: the Ringleader and the Solution.Clinical reviews in allergy & immunology · 2022Review
- Androgen-Mediated Anti-inflammatory Cellular Processes as Therapeutic Targets in Lupus.Frontiers in immunology · 2020Review
- B Cell Abnormalities in Systemic Lupus Erythematosus and Lupus Nephritis-Role in Pathogenesis and Effect of Immunosuppressive Treatments.International journal of molecular sciences · 2019Review
- New insights into the role of renal resident cells in the pathogenesis of lupus nephritis.The Korean journal of internal medicine · 2018Review
- Novel Treatments in Lupus.Frontiers in immunology · 2018Review
- The classic signalling and trans-signalling of interleukin-6 are both injurious in podocyte under high glucose exposure.Journal of cellular and molecular medicine · 2018Article
- Cytokine profile in childhood-onset systemic lupus erythematosus: a cross-sectional and longitudinal study.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2017Article
- Biologics for the treatment of autoimmune renal diseases.Nature reviews. Nephrology · 2016Review
- Nuclear Factor Erythroid 2-Related Factor 2 Drives Podocyte-Specific Expression of Peroxisome Proliferator-Activated Receptor γ Essential for Resistance to Crescentic GN.Journal of the American Society of Nephrology : JASN · 2016Article
- Current and emerging treatment options in the management of lupus.ImmunoTargets and therapy · 2016Review
- IL-6 Trans-Signaling Drives Murine Crescentic GN.Journal of the American Society of Nephrology : JASN · 2016Article
- Human embryonic stem cell-derived mesenchymal cells preserve kidney function and extend lifespan in NZB/W F1 mouse model of lupus nephritis.Scientific reports · 2015Article
- Key issues in the management of patients with systemic lupus erythematosus: latest developments and clinical implications.Therapeutic advances in musculoskeletal disease · 2015Review
- Inflammation-Induced IL-6 Functions as a Natural Brake on Macrophages and Limits GN.Journal of the American Society of Nephrology : JASN · 2015Article
- Article
- Lupus nephritis: the evolving role of novel therapeutics.American journal of kidney diseases : the official journal of the National Kidney Foundation · 2014Review
- Estrogen Receptor Alpha Binding to ERE is Required for Full Tlr7- and Tlr9-Induced Inflammation.SOJ immunology · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ability of interleukin-6 (IL-6) to modulate immune parameters and mesangial cell function suggests a role for this cytokine in the development of autoimmune glomerulonephritis. This hypothesis was tested in 6-month-old female (NZB x NZW)F1 mice that were administered recombinant human IL-6 (rhIL-6) (50 and 250 micrograms/kg s.c.) for 12 weeks, resulting in an accelerated and severe form of membranoproliferative glomerulonephritis associated with marked upregulation of mesangial major histocompatibility complex class II antigen and glomerular ICAM-1 expression. To distinguish direct effects of rhIL-6 on the renal mesangium from those mediated through the immune system, (NZB x NZW)F1 mice were immunosuppressed with cyclosporin. Immunosuppression by cyclosporin inhibited the development of glomerulonephritis, decreased class II antigen expression, and abrogated IL-6-mediated effects. Administration of neutralizing anti-IL-6 antibody had no effect on the spontaneous development of glomerulonephritis in (NZB x NZW)F1 mice. This finding, together with undetectable IL-6 serum levels, makes a pathogenetic role of endogenously produced IL-6 in this disease model unlikely. In contrast to (NZB x NZW)F1 mice, parental NZW or BALB/c mice given high doses of rhIL-6 (500 micrograms/kg) or recombinant murine IL-6 (100 micrograms/kg) daily for 4 weeks failed to develop morphological or biochemical evidence of glomerulonephritis. Induction of acute phase proteins, anemia, thrombocytosis, and induction of renal class II antigen confirmed the biological activity of IL-6 in these mice. In conclusion, while non-nephritogenic in normal mice, IL-6 accelerates the development of the genetically determined glomerulonephritis of (NZB x NZW)F1 mice through effects mediated by a modulated immune system. Since neutralizing IL-6 antibody treatment did not prevent the development of glomerulonephritis, it is unlikely that increased IL-6 production plays a role in the pathogenesis of lupus nephritis.
Indexed as
Identifiers
8178944PMC1887352W1867937417What OpenQuestion holds
Registered trials
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