ArticleArthritis & rheumatology (Hoboken, N.J.)2014
Toll-like receptor 7-stimulated tumor necrosis factor α causes bone marrow damage in systemic lupus erythematosus.
Article in Arthritis & rheumatology (Hoboken, N.J.), 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 56 citations in OpenAlex.
- Whole blood exchange-lymphoplasmapheresis combined transfusion as an immunotherapy in systemic lupus erythematosus.iScience · 2026Article
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- Evidence that autoantibody production may be driven by acute Epstein-Barr virus infection in Sjögren's disease.Annals of the rheumatic diseases · 2024Article
- MEK1/2- and ERK1/2-Mediated Lung Endothelial Injury and Altered Hemostasis Promote Diffuse Alveolar Hemorrhage in Murine Lupus.Arthritis & rheumatology (Hoboken, N.J.) · 2024Article
- Human TLR8 induces inflammatory bone marrow erythromyeloblastic islands and anemia in SLE-prone mice.Life science alliance · 2023Article
- Th1-related transcription factors and cytokines in systemic lupus erythematosus.Frontiers in immunology · 2023Review
- Glutathione peroxidase 4-regulated neutrophil ferroptosis induces systemic autoimmunity.Nature immunology · 2021Article
- Overexpression of cathepsin S exacerbates lupus pathogenesis through upregulation TLR7 and IFN-α in transgenic mice.Scientific reports · 2021Article
- Patrolling human SLE haematopoietic progenitors demonstrate enhanced extramedullary colonisation; implications for peripheral tissue injury.Scientific reports · 2021Article
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- Common innate pathways to autoimmune disease.Clinical immunology (Orlando, Fla.) · 2020Review
- Type 1 Interferon Gene Signature Promotes RBC Alloimmunization in a Lupus Mouse Model.Frontiers in immunology · 2020Article
- The Innate Immune Response to Infection Induces Erythropoietin-Dependent Replenishment of the Dendritic Cell Compartment.Frontiers in immunology · 2020Article
- Alpha-1-Antitrypsin Ameliorates Pristane Induced Diffuse Alveolar Hemorrhage in Mice.Journal of clinical medicine · 2019Article
- High-dimensional analysis reveals a pathogenic role of inflammatory monocytes in experimental diffuse alveolar hemorrhage.JCI insight · 2019Article
- Control of TLR7-mediated type I IFN signaling in pDCs through CXCR4 engagement-A new target for lupus treatment.Science advances · 2019Article
- Pathogenesis and treatment of autoimmune rheumatic diseases.Current opinion in rheumatology · 2019Review
- TLR7-Mediated Lupus Nephritis Is Independent of Type I IFN Signaling.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Toll-like receptors in lupus nephritis.Journal of biomedical science · 2018Review
- CD38 promotes pristane-induced chronic inflammation and increases susceptibility to experimental lupus by an apoptosis-driven and TRPM2-dependent mechanism.Scientific reports · 2018Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
objectiveTo define the pathogenesis of bone marrow (BM) involvement in systemic lupus erythematosus (SLE).
methodsTumor necrosis factor α (TNFα) levels, cell death, and cellular damage in BM from SLE patients, controls, and mice with pristane-induced lupus were analyzed using a morphometric technique and immunohistochemistry. The pathogenesis of BM abnormalities was studied in wild-type (WT), TNFα(-/-) , Toll-like receptor-deficient (TLR-7(-/-) ), interferon (IFN)-α/β/ω receptor-knockout (IFNAR(-/-) ), and B cell-deficient (μmt) mice treated with pristane. Flow cytometry was used to examine TNFα production (by intracellular staining) and plasma cell/plasmablast development. CXCL12 expression was determined by quantitative polymerase chain reaction.
resultsBM from SLE patients exhibited striking death of niche and hematopoietic cells associated with TNFα overproduction. BM from mice with a type I IFN-mediated lupus syndrome induced by pristane showed similar abnormalities. TNFα was produced mainly by BM neutrophils, many with phagocytosed nuclear material (lupus erythematosus cells). TNFα production was abolished in pristane-treated TLR-7(-/-) and μmt mice but was restored in μmt mice by infusing normal plasma. Pristane-treated WT and IFNAR(-/-) mice developed anemia, BM hypocellularity, and extramedullary hematopoiesis, which were absent in TLR-7(-/-) and TNFα(-/-) mice. Additionally, the expression of CXCL12, which is produced by stromal cells and mediates homing of hematopoietic cells and plasmablasts, was decreased in BM from pristane-treated WT mice but was normal in BM from pristane-treated TNFα(-/-) mice.
conclusionAlthough autoantibodies and glomerulonephritis are type I IFN dependent, lupus-associated BM abnormalities were TLR-7 and TNFα driven but type I IFN independent, suggesting that lupus is a disorder of innate immunity in which TLR-7 activation by phagocytosed nuclei causes relentless type I IFN and TNFα production mediating glomerulonephritis and hematologic involvement, respectively.
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