ArticleBMC immunology2010
Lack of the pattern recognition molecule mannose-binding lectin increases susceptibility to influenza A virus infection.
Article in BMC immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 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.
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
43 citing papers in PubMed, 70 citations in OpenAlex.
- Evaluation of Mannose Binding Lectin Gene Variants in Pediatric Influenza Virus-Related Critical Illness.Frontiers in immunology · 2019Trial
- Elevated plasma CL-K1 level is associated with a risk of developing disseminated intravascular coagulation (DIC).Journal of thrombosis and thrombolysis · 2014Trial
- Yersinia enterocolitica O:3 Outer Membrane Vesicles as a Platform for Complement Activation.Journal of extracellular vesicles · 2026Article
- The Biological Role of Enveloped Virus Glycosylation and Its Interactions with Antiviral Lectins.Advances in experimental medicine and biology · 2026Review
- Circulating mannose-binding lectin in diabetic patients and risk of vascular complications: a systematic review and meta-analysis.Journal of diabetes and metabolic disorders · 2024Article
- A B cell screen against endogenous retroviruses identifies glycan-reactive IgM that recognizes a broad array of enveloped viruses.Science immunology · 2024Article
- The complement system and human autoimmune diseases.Journal of autoimmunity · 2023Review
- Complement as a vital nexus of the pathobiological connectome for acute respiratory distress syndrome: An emerging therapeutic target.Frontiers in immunology · 2023Review
- MBL Binding with AhR Controls Th17 Immunity in Silicosis-Associated Lung Inflammation and Fibrosis.Journal of inflammation research · 2022Article
- Review
- Review
- A cross-neutralizing antibody between HIV-1 and influenza virus.PLoS pathogens · 2021Article
- Altered glycosylation of IgG4 promotes lectin complement pathway activation in anti-PLA2R1-associated membranous nephropathy.The Journal of clinical investigation · 2021Article
- Adjuvanticity of ProcessedImmune network · 2020Article
- Self-assembling influenza nanoparticle vaccines drive extended germinal center activity and memory B cell maturation.JCI insight · 2020Article
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Why Glycosylation Matters in Building a Better Flu Vaccine.Molecular & cellular proteomics : MCP · 2019Review
- Microarray analysis of infectious bronchitis virus infection of chicken primary dendritic cells.BMC genomics · 2019Article
- Influenza virus N-linked glycosylation and innate immunity.Bioscience reports · 2019Review
- Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis.mBio · 2018Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
backgroundMannose-binding lectin (MBL), a pattern recognition innate immune molecule, inhibits influenza A virus infection in vitro. MBL deficiency due to gene polymorphism in humans has been associated with infection susceptibility. These clinical observations were confirmed by animal model studies, in which mice genetically lacking MBL were susceptible to certain pathogens, including herpes simplex virus 2.
resultsWe demonstrate that MBL is present in the lung of naïve healthy wild type (WT) mice and that MBL null mice are more susceptible to IAV infection. Administration of recombinant human MBL (rhMBL) reverses the infection phenotype, confirming that the infection susceptibility is MBL-mediated. The anti-viral mechanisms of MBL include activation of the lectin complement pathway and coagulation, requiring serum factors. White blood cells (WBCs) in the lung increase in WT mice compared with MBL null mice on day 1 post-infection. In contrast, apoptotic macrophages (MΦs) are two-fold higher in the lung of MBL null mice compared with WT mice. Furthermore, MBL deficient macrophages appear to be susceptible to apoptosis in vitro. Lastly, soluble factors, which are associated with lung injury, are increased in the lungs of MBL null mice during IAV infection. These results suggest that MBL plays a key role against IAV infection.
conclusionMBL plays a key role in clearing IAV and maintaining lung homeostasis. In addition, our findings also suggest that MBL deficiency maybe a risk factor in IAV infection and MBL may be a useful adjunctive therapy for IAV infection.
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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.