ArticleFrontiers in immunology2023
Loss of interleukin-1 beta is not protective in the lupus-prone NZM2328 mouse model.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 9 citations in OpenAlex.
- NOX2 deficiency exacerbates lupus nephritis through activation of NLRP3 inflammasome in neutrophils.Journal of biomedical science · 2026Article
- Interleukin-1β and MicroRNA-146a as Prognostic and Diagnostic Markers of Systemic Lupus Erythematosus Complexity.Iranian journal of pathology · 2026Article
- Recent insights into the role of innate immunity in lupus.Human molecular genetics · 2025Review
- Lupus-prone NZM2328 mice exhibit enhanced UV-induced myeloid cell recruitment and activation in a type I interferon dependent manner.Journal of autoimmunity · 2024Article
- STAT1 aggravates kidney injury by NOD-like receptor (NLRP3) signaling in MRL-lpr mice.Journal of molecular histology · 2024Article
- Assessment of the role of high-density lipoproteins and their immunomodulatory activity in systemic lupus erythematosus immunopathology.Lupus science & medicine · 2024Article
- The STING inhibitor (ISD-017) reduces glomerulonephritis in 129.B6.Fcgr2b-deficient mice.Scientific reports · 2024Article
- B cell-intrinsic Myd88 regulates disease progression in murine lupus.The Journal of experimental medicine · 2023Article
- New Potentiality of Bioactive Substances: Regulating the NLRP3 Inflammasome in Autoimmune Diseases.Nutrients · 2023Review
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Aberrant activation of the innate immune system is a known driver of lupus pathogenesis. Inhibition of the inflammasome and its downstream signaling components in murine models of lupus has been shown to reduce the severity of disease. Interleukin-1 beta (IL-1β) is a proinflammatory cytokine released from cells following inflammasome activation. Here, we examine how loss of IL-1β affects disease severity in the lupus-prone NZM2328 mouse model. We observed a sex-biased increase in immune complex deposition in the kidneys of female mice in the absence of IL-1β that corresponds to worsened proteinuria. Loss of IL-1β did not result in changes in overall survival, anti-dsDNA autoantibody production, or renal immune cell infiltration. RNA-sequencing analysis identified upregulation of TNF and IL-17 signaling pathways specifically in females lacking IL-1β. Increases in these signaling pathways were also found in female patients with lupus nephritis, suggesting clinical relevance for upregulation of these pathways. Together, these data suggest that inhibition of the inflammasome or its downstream elements that block IL-1β signaling may need to be approached with caution in SLE, especially in patients with renal involvement to prevent potential disease exacerbation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.