ArticleInfection and immunity2004
Complement protein C3 binding to Mycobacterium tuberculosis is initiated by the classical pathway in human bronchoalveolar lavage fluid.
Article in Infection and immunity, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.
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Who cites it
64 citing papers in PubMed, 129 citations in OpenAlex.
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- Clinical manifestations and immune response to tuberculosis.World journal of microbiology & biotechnology · 2023Review
- Complement regulatory proteins: Candidate biomarkers in differentiating tuberculosis pleural effusion.Frontiers in immunology · 2023Article
- Tuberculosis and COVID-19 in the elderly: factors driving a higher burden of disease.Frontiers in immunology · 2023Review
- Low serum complement level is associated with higher mortality in tuberculous meningitis: a retrospective cohort study.Encephalitis (Seoul, Korea) · 2023Article
- Alternative translation and retrotranslocation of cytosolic C3 that detects cytoinvasive bacteria.Cellular and molecular life sciences : CMLS · 2022Article
- Association Between Plasma Exosomes S100A9/C4BPA and Latent Tuberculosis Infection Treatment: Proteomic Analysis Based on a Randomized Controlled Study.Frontiers in microbiology · 2022Article
- Pathogenesis of SARS-CoV-2 andFrontiers in immunology · 2022Review
- Complement receptor 3 mediatesVirulence · 2021Article
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- Exploring the Use of Medicinal Plants and Their Bioactive Derivatives as Alveolar NLRP3 Inflammasome Regulators duringInternational journal of molecular sciences · 2021Review
- Anaphylatoxins orchestrate Th17 response via interactions between CD16+ monocytes and pleural mesothelial cells in tuberculous pleural effusion.PLoS neglected tropical diseases · 2021Article
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- Analysis of complement deposition and processing on Chlamydia trachomatis.Medical microbiology and immunology · 2021Article
- The Role of Complement System and the Immune Response to Tuberculosis Infection.Medicina (Kaunas, Lithuania) · 2021Review
- Innate Immune Pattern Recognition Receptors of Mycobacterium tuberculosis: Nature and Consequences for Pathogenesis of Tuberculosis.Advances in experimental medicine and biology · 2021Article
- Complement Component C1q as an Emerging Biomarker for the Diagnosis of Tuberculous Pleural Effusion.Frontiers in microbiology · 2021Article
4 more citing papers are in PubMed but not listed here.
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PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
In high concentrations of fresh nonimmune human serum, Mycobacterium tuberculosis activates the alternative pathway of complement and binds C3 protein, resulting in enhanced phagocytosis by complement receptors on human alveolar macrophages. Yet in the lung, the alternative pathway of complement is relatively inactive compared to the classical pathway. To begin to determine whether C3 opsonophagocytosis of M. tuberculosis by alveolar macrophages can occur in the lung of the immunologically naive host, we characterized the binding of C3 to M. tuberculosis in different concentrations of fresh nonimmune human serum and concentrated human bronchoalveolar lavage fluid. Here we show that in human serum, C3 binding to M. tuberculosis is rapid, initiated by either the alternative pathway or the classical pathway, depending on the concentration of serum, and occurs by covalent linkages between the bacterial surface and the C3 cleavage products, C3b or C3bi. Human bronchoalveolar lavage fluid contains C3 protein and functional classical pathway activity that mediates the binding of C3 to the surface of M. tuberculosis. These studies provide evidence that when M. tuberculosis is first inhaled into the lungs of the human host, the bacterium is opsonized by C3 cleavage via classical pathway activation within the alveolus, providing a C3-dependent entry pathway into resident alveolar macrophages.
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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.