ArticleProceedings of the National Academy of Sciences of the United States of America2014
Inflammasome-independent IL-1β mediates autoinflammatory disease in Pstpip2-deficient mice.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.
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Who cites it
66 citing papers in PubMed, 122 citations in OpenAlex.
- Review
- IL-1 family cytokines in inflammation and immunity.Cellular & molecular immunology · 2025Review
- Disruption of Morrbid alleviates autoinflammatory osteomyelitis in Pstpip2-deficient mice.Disease models & mechanisms · 2025Article
- Neutrophil extracellular traps and interleukin-1β in cystic fibrosis lung disease.Frontiers in immunology · 2025Review
- An improved understanding of pediatric chronic nonbacterial osteomyelitis pathophysiology informs current and future treatment.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2024Review
- Advances of the multifaceted functions of PSTPIP2 in inflammatory diseases.Frontiers in immunology · 2024Review
- Current and future advances in practice: SAPHO syndrome and chronic non-bacterial osteitis (CNO).Rheumatology advances in practice · 2024Review
- Chronic inflammation decreases HSC fitness by activating the druggable Jak/Stat3 signaling pathway.EMBO reports · 2023Article
- Chronic Recurrent Multifocal Osteomyelitis (CRMO) and Juvenile Spondyloarthritis (JSpA): To What Extent Are They Related?Journal of clinical medicine · 2023Article
- Bile acids induce IL-1α and drive NLRP3 inflammasome-independent production of IL-1β in murine dendritic cells.Frontiers in immunology · 2023Article
- Immunomodulatory roles of metalloproteinases in rheumatoid arthritis.Frontiers in pharmacology · 2023Review
- Pediatric autoinflammatory bone disorders-a mini review with special focus on pathogenesis and inborn errors of immunity.Frontiers in pediatrics · 2023Review
- Pyoderma gangrenosum following anti-TNF therapy in chronic recurrent multifocal osteomyelitis: drug reaction or cutaneous manifestation of the disease? A critical review on the topic with an emblematic case report.Frontiers in medicine · 2023Review
- Autoinflammatory manifestations in adult patients.Clinical and experimental immunology · 2022Article
- Review
- Analysis of the fecal and oral microbiota in chronic recurrent multifocal osteomyelitis.Arthritis research & therapy · 2022Article
- Determining distinct roles of IL-1α through generation of an IL-1α knockout mouse with no defect in IL-1β expression.Frontiers in immunology · 2022Article
- Molecular interactions of adaptor protein PSTPIP2 control neutrophil-mediated responses leading to autoinflammation.Frontiers in immunology · 2022Article
- Chronic recurrent multifocal osteomyelitis. A narrative and pictorial review.Frontiers in immunology · 2022Review
- Article
6 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 7 institutions in 3 countries.
Funding
Abstract
Chronic recurrent multifocal osteomyelitis (CRMO) is a human autoinflammatory disorder that primarily affects bone. Missense mutation (L98P) of proline-serine-threonine phosphatase-interacting protein 2 (Pstpip2) in mice leads to a disease that is phenotypically similar to CRMO called chronic multifocal osteomyelitis (cmo). Here we show that deficiency of IL-1RI in cmo mice resulted in a significant reduction in the time to onset of disease as well as the degree of bone pathology. Additionally, the proinflammatory cytokine IL-1β, but not IL-1α, played a critical role in the pathology observed in cmo mice. In contrast, disease in cmo mice was found to be independent of the nucleotide-binding domain, leucine-rich repeat-containing family, pyrin domain-containing 3 (NLRP3) inflammasome as well as caspase-1. Neutrophils, but not bone marrow-derived macrophages, from cmo mice secreted increased IL-1β in response to ATP, silica, and Pseudomonas aeruginosa compared with neutrophils from WT mice. This aberrant neutrophil response was sensitive to inhibition by serine protease inhibitors. These results demonstrate an inflammasome-independent role for IL-1β in disease progression of cmo and implicate neutrophils and neutrophil serine proteases in disease pathogenesis. These data provide a rationale for directly targeting IL-1RI or IL-1β as a therapeutic strategy in CRMO.
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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.