ArticleJournal of immunology (Baltimore, Md. : 1950)2016
C1q Modulates the Response to TLR7 Stimulation by Pristane-Primed Macrophages: Implications for Pristane-Induced Lupus.
Article in Journal of immunology (Baltimore, Md. : 1950), 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 23 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Multiple-omics analysis reveals a dedifferentiation-immune loop in intrahepatic cholangiocarcinoma.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- [Correlation of anti-C1q antibodies with active systemic lupus erythematosus and lupus nephritis in children].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2024Article
- Type I IFN in Glomerular Disease: Scarring beyond the STING.International journal of molecular sciences · 2024Review
- Deconvolution of synovial myeloid cell subsets across pathotypes and role of COL3A1+ macrophages in rheumatoid arthritis remission.Frontiers in immunology · 2024Article
- Comprehensive analysis of IRF8-related genes and immune characteristics in lupus nephritis.Frontiers in pharmacology · 2024Article
- Multi-omics profiling identifies C1QA/BAnnals of translational medicine · 2022Article
- R848 or influenza virus can induce potent innate immune responses in the lungs of neonatal mice.Mucosal immunology · 2021Article
- Tissue-resident macrophages actively suppress IL-1beta release via a reactive prostanoid/IL-10 pathway.The EMBO journal · 2020Article
- Retinoic Acid Exerts Disease Stage-Dependent Effects on Pristane-Induced Lupus.Frontiers in immunology · 2020Article
- Early Peritoneal CC Chemokine Production Correlates with Divergent Inflammatory Phenotypes and Susceptibility to Experimental Arthritis in Mice.Journal of immunology research · 2019Article
- Pristane-induced lupus: considerations on this experimental model.Clinical rheumatology · 2017Review
- Myeloid Populations in Systemic Autoimmune Diseases.Clinical reviews in allergy & immunology · 2017Review
- Local amplifiers of IL-4Rα-mediated macrophage activation promote repair in lung and liver.Science (New York, N.Y.) · 2017Article
- Notch-Hes-1 axis controls TLR7-mediated autophagic death of macrophage via induction of P62 in mice with lupus.Cell death & disease · 2016Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
The complement component C1q is known to play a controversial role in the pathogenesis of systemic lupus erythematosus, but the underlying mechanisms remain poorly understood. Intraperitoneal injection of pristane induces a lupus-like syndrome whose pathogenesis implicates the secretion of type I IFN by CD11b(+) Ly6C(high) inflammatory monocytes in a TLR7-dependent fashion. C1q was also shown to influence the secretion of IFN-α. In this study, we explored whether C1q deficiency could affect pristane-induced lupus. Surprisingly, C1qa(-/-) mice developed lower titers of circulating Abs and milder arthritis compared with the controls. In keeping with the clinical scores, 2 wk after pristane injection the peritoneal recruitment of CD11b(+) Ly6C(high) inflammatory monocytes in C1qa(-/-) mice was impaired. Furthermore, C1q-deficient pristane-primed resident peritoneal macrophages secreted significantly less CCL3, CCL2, CXCL1, and IL-6 when stimulated in vitro with TLR7 ligand. Replenishing C1q in vivo during the pristane-priming phase rectified this defect. Conversely, pristane-primed macrophages from C3-deficient mice did not show impaired cytokine production. These findings demonstrate that C1q deficiency impairs the TLR7-dependent chemokine production by pristane-primed peritoneal macrophages and suggest that C1q, and not C3, is involved in the handling of pristane by phagocytic cells, which is required to trigger disease in this model.
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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.