ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
35 citing papers in PubMed, 57 citations in OpenAlex.
- scVAEDer: integrating deep diffusion models and variational autoencoders for single-cell transcriptomics analysis.Genome biology · 2025Article
- Emerging concepts and treatments in autoinflammatory interferonopathies and monogenic systemic lupus erythematosus.Nature reviews. Rheumatology · 2025Review
- Identifying selection signatures for immune response and resilience to Aleutian disease in mink using genotype data.Frontiers in genetics · 2024Article
- Genetics of SLE: mechanistic insights from monogenic disease and disease-associated variants.Nature reviews. Nephrology · 2023Review
- Development and function of chicken XCR1Frontiers in immunology · 2023Article
- Mitochondrial protein CMPK2 regulates IFN alpha-enhanced foam cell formation, potentially contributing to premature atherosclerosis in SLE.Arthritis research & therapy · 2021Article
- Autoantibodies against complement component C1q in systemic lupus erythematosus.Clinical & translational immunology · 2021Review
- SLE: Novel Postulates for Therapeutic Options.Frontiers in immunology · 2020Review
- Proinflammatory Differentiation of Macrophages Through Microparticles That Form Immune Complexes Leads to T- and B-Cell Activation in Systemic Autoimmune Diseases.Frontiers in immunology · 2019Article
- Rheumatoid arthritis and systemic lupus erythematosus: Pathophysiological mechanisms related to innate immune system.SAGE open medicine · 2019Review
- A Bayesian gene network reveals insight into the JAK-STAT pathway in systemic lupus erythematosus.PloS one · 2019Article
- MafB is a critical regulator of complement component C1q.Nature communications · 2017Article
- C1q: A fresh look upon an old molecule.Molecular immunology · 2017Review
- Death receptor 6 contributes to autoimmunity in lupus-prone mice.Nature communications · 2017Article
- C1q Modulates the Response to TLR7 Stimulation by Pristane-Primed Macrophages: Implications for Pristane-Induced Lupus.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Uncoupling complement C1s activation from C1q binding in apoptotic cell phagocytosis and immunosuppressive capacity.Clinical immunology (Orlando, Fla.) · 2016Article
- Breakdown of Immune Tolerance in Systemic Lupus Erythematosus by Dendritic Cells.Journal of immunology research · 2016Review
- A curated compendium of monocyte transcriptome datasets of relevance to human monocyte immunobiology research.F1000Research · 2016Article
- A compendium of monocyte transcriptome datasets to foster biomedical knowledge discovery.F1000Research · 2016Article
- Widely divergent transcriptional patterns between SLE patients of different ancestral backgrounds in sorted immune cell populations.Journal of autoimmunity · 2015Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Immune complexes (ICs) play a pivotal role in causing inflammation in systemic lupus erythematosus (SLE). Yet, it remains unclear what the dominant blood cell type(s) and inflammation-related gene programs stimulated by lupus ICs are. To address these questions, we exposed normal human PBMCs or CD14(+) isolated monocytes to SLE ICs in the presence or absence of C1q and performed microarray analysis and other tests for cell activation. By microarray analysis, we identified genes and pathways regulated by SLE ICs that are both type I IFN dependent and independent. We also found that C1q-containing ICs markedly reduced expression of the majority of IFN-response genes and also influenced the expression of multiple other genes induced by SLE ICs. Surprisingly, IC activation of isolated CD14(+) monocytes did not upregulate CD40 and CD86 and only modestly stimulated inflammatory gene expression. However, when monocyte subsets were purified and analyzed separately, the low-abundance CD14(dim) ("patrolling") subpopulation was more responsive to ICs. These observations demonstrate the importance of plasmacytoid dendritic cells, CD14(dim) monocytes, and C1q as key regulators of inflammatory properties of ICs and identify many pathways through which they act.
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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.