ArticleBlood2009
Primed innate immunity leads to autoinflammatory disease in PSTPIP2-deficient cmo mice.
Article in Blood, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed.
- HSPCs and TScience advances · 2026Article
- Article
- Disruption of Morrbid alleviates autoinflammatory osteomyelitis in Pstpip2-deficient mice.Disease models & mechanisms · 2025Article
- Update on the diagnosis and treatment of CNO in children: a clinician's perspective.European journal of pediatrics · 2024Review
- Implications of inflammatory cell death-PANoptosis in health and disease.Archives of pharmacal research · 2024Review
- Advances of the multifaceted functions of PSTPIP2 in inflammatory diseases.Frontiers in immunology · 2024Review
- Chronic Non-bacterial Osteomyelitis (CNO) In Childhood: A Review.Current pediatric reviews · 2024Review
- Fathers' preconception smoking and offspring DNA methylation.Clinical epigenetics · 2023Article
- Chronic inflammation decreases HSC fitness by activating the druggable Jak/Stat3 signaling pathway.EMBO reports · 2023Article
- 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
- PSTPIP2 regulates synovial macrophages polarization and dynamics via ERβ in the joint microenvironment.Arthritis research & therapy · 2022Article
- Molecular interactions of adaptor protein PSTPIP2 control neutrophil-mediated responses leading to autoinflammation.Frontiers in immunology · 2022Article
- Role of the F-BAR Family Member PSTPIP2 in Autoinflammatory Diseases.Frontiers in immunology · 2021Review
- PSTPIP2 inhibits cisplatin-induced acute kidney injury by suppressing apoptosis of renal tubular epithelial cells.Cell death & disease · 2020Article
- Chronic non-bacterial osteomyelitis and autoinflammatory bone diseases.Clinical immunology (Orlando, Fla.) · 2020Review
- The nonreceptor tyrosine kinase SYK drives caspase-8/NLRP3 inflammasome-mediated autoinflammatory osteomyelitis.The Journal of biological chemistry · 2020Article
- Mast cells enhance sterile inflammation in chronic nonbacterial osteomyelitis.Disease models & mechanisms · 2019Article
- PSTPIP2 Inhibits the Inflammatory Response and Proliferation of Fibroblast-Like SynoviocytesFrontiers in pharmacology · 2018Article
- Function and regulation of IL-1α in inflammatory diseases and cancer.Immunological reviews · 2018Review
Corrections and comments
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Authors and funding
8 authors.
Funding
Abstract
The mouse Lupo (I282N) mutation in proline-serine-threonine phosphatase-interacting protein 2 (PSTPIP2) leads to reduced expression of PSTPIP2 that is associated with a macrophage-mediated autoinflammatory disease. Another mutation in PSTPIP2, L98P, termed chronic multifocal osteomyelits (cmo), leads to a disease in mice that resembles chronic recurrent multifocal osteomyelits in humans. The cellular basis of cmo disease was investigated. cmo disease develops independently of lymphocytes and is cured by bone marrow transplantation. Macrophages, mast cells, and osteoclasts from cmo mice fail to express detectable PSTPIP2 protein. Asymptomatic Pstpip2(cmo/cmo) mice have increased circulating levels of macrophage inflammatory protein 1-alpha and interleukin-6, and their macrophages exhibit increased production of these inflammatory mediators, which is normalized by retroviral expression of wild-type PSTPIP2. Spleens of asymptomatic cmo mice contain increased numbers of macrophage precursors, and cmo mice mobilize more macrophage precursors in response to a sterile inflammatory stimulus. Signal transducer and activator of transcription 1 is elevated in cmo splenic macrophages, which also exhibit increased colony-stimulating factor-1-stimulated proliferation and increased extracellular signal-regulated kinase 1/2 phosphorylation. PSTPIP2 overexpression in macrophages leads to the opposite phenotype. Thus, PSTPIP2 deficiency causes both an expansion of macrophage progenitors and increased responsiveness of mature macrophages to activating stimuli, which together prime the organism for exaggerated and sustained responses leading to autoinflammatory disease.
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