ArticleJCI insight2019
Cigarette smoke-induced reduction of C1q promotes emphysema.
Article in JCI insight, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
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
26 citing papers in PubMed, 1 synthesis or guideline pooled it, 44 citations in OpenAlex.
- C1q as a target molecule to treat human disease: What do mouse studies teach us?Frontiers in immunology · 2022Pooled it
- Identification of HIF1A as a therapeutic target during SARS-CoV-2-associated lung injury.JCI insight · 2025Trial
- The Convergent Immunopathogenesis of Cigarette Smoke Exposure: From Oxidative Stress to Epigenetic Reprogramming in Chronic Disease.International journal of molecular sciences · 2025Review
- Emerging roles for complement in lung transplantation.The Journal of clinical investigation · 2025Review
- Impact of smoking on the complement system: a narrative review.Frontiers in immunology · 2025Review
- The role of complement C1q in atrial fibrillation: a marker for disease progression and surgical outcomes.Frontiers in cardiovascular medicine · 2025Article
- Identification of Dendritic Cell-Associated Genes in COPD Based on Bioinformatics.International journal of chronic obstructive pulmonary disease · 2025Article
- Validation of Systemic Complement Signatures in the Progression of Chronic Obstructive Pulmonary Disease.American journal of respiratory and critical care medicine · 2024Article
- A model of dysregulated crosstalk between dendritic, natural killer, and regulatory T cells in chronic obstructive pulmonary disease.Trends in immunology · 2024Article
- Downregulation ofeLife · 2024Article
- Downregulation ofbioRxiv : the preprint server for biology · 2024Article
- Complement C1q is a key player in tumor-associated macrophage-mediated CD8International journal of biological sciences · 2024Article
- Different Transcriptome Features of Peripheral Blood Mononuclear Cells in Non-Emphysematous Chronic Obstructive Pulmonary Disease.International journal of molecular sciences · 2023Article
- Complement in Human Brain Health: Potential of Dietary Food in Relation to Neurodegenerative Diseases.Foods (Basel, Switzerland) · 2023Review
- Contribution of adaptive immunity to human COPD and experimental models of emphysema.Physiological reviews · 2023Review
- Severity of Lung Function Impairment Drives Transcriptional Phenotypes of COPD and Relates to Immune and Metabolic Processes.International journal of chronic obstructive pulmonary disease · 2023Article
- Chronic exposure to carbon black ultrafine particles reprograms macrophage metabolism and accelerates lung cancer.Science advances · 2022Article
- Alternative adenosine Receptor activation: The netrin-Adora2b link.Frontiers in pharmacology · 2022Review
- Associative analysis of multi-omics data indicates that acetylation modification is widely involved in cigarette smoke-induced chronic obstructive pulmonary disease.Frontiers in medicine · 2022Article
- Hypoxia-inducible factor-dependent induction of myeloid-derived netrin-1 attenuates natural killer cell infiltration during endotoxin-induced lung injury.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2021Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 1 country.
Funding
Abstract
Alteration of innate immune cells in the lungs can promote loss of peripheral tolerance that leads to autoimmune responses in cigarette smokers. Development of autoimmunity in smokers with emphysema is also strongly linked to the expansion of autoreactive T helper (Th) cells expressing interferon gamma (Th1), and interleukin 17A (Th17). However, the mechanisms responsible for enhanced self-recognition and reduced immune tolerance in smoker with emphysema remain less clear. Here we show that C1q, a component of the complement protein 1 complex (C1), is downregulated in lung CD1a+ antigen presenting cells (APCs) isolated from emphysematous human, and mouse lung APCs after chronic cigarette smoke exposure. C1q potentiated the function of APCs to differentiate CD4+ T cells to Tregs, while it inhibited Th17 cell development and proliferation. Mice deficient in C1q that were exposed to chronic smoke exhibited exaggerated lung inflammation marked by increased Th17 cells, while reconstitution of C1q in the lungs enhanced Tregs abundance, dampened smoke-induced lung inflammation, and reversed established emphysema. Our findings demonstrate that cigarette smoke-mediated loss of C1q could play a key role in reduced peripheral tolerance, which could be explored to treat emphysema.
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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.