ArticleClinical and experimental immunology2014
Interaction of lectin pathway of complement-activating pattern recognition molecules with mycobacteria.
Article in Clinical and experimental immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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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
22 citing papers in PubMed, 35 citations in OpenAlex.
- Complement Dysregulation in Kidney Diseases: Mechanisms, Biomarkers, and Emerging Targeted Therapies.International journal of molecular sciences · 2026Review
- The value of LAM and LprG in extracellular vesicles in the diagnostic and therapeutic field of renal tuberculosis.Frontiers in tuberculosis · 2025Review
- Role of pattern recognition receptors in sensingHeliyon · 2023Review
- Article
- Article
- 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
- Underwhelming or Misunderstood? Genetic Variability of Pattern Recognition Receptors in Immune Responses and Resistance toFrontiers in immunology · 2021Review
- ITIH4 acts as a protease inhibitor by a novel inhibitory mechanism.Science advances · 2021Article
- Human Neutrophil Granule Exocytosis in Response toPathogens (Basel, Switzerland) · 2020Article
- Collectins: Innate Immune Pattern Recognition Molecules.Advances in experimental medicine and biology · 2020Review
- Myeloid C-Type Lectin Receptors in Tuberculosis and HIV Immunity: Insights Into Co-infection?Frontiers in cellular and infection microbiology · 2020Review
- Ficolins and the Recognition of Pathogenic Microorganisms: An Overview of the Innate Immune Response and Contribution of Single Nucleotide Polymorphisms.Journal of immunology research · 2019Review
- Mannose-binding lectin (MBL) deficiency and tuberculosis infection in patients with ankylosing spondylitis.Clinical rheumatology · 2018Article
- AmpliSeq Screening of Genes Encoding the C-Type Lectin Receptors and Their Signaling Components Reveals a Common Variant inFrontiers in immunology · 2018Article
- Review
- Mannose-Binding Lectin: Biologic Characteristics and Role in the Susceptibility to Infections and Ischemia-Reperfusion Related Injury in Critically Ill Neonates.Journal of immunology research · 2017Review
- Evasion Mechanisms Used by Pathogens to Escape the Lectin Complement Pathway.Frontiers in microbiology · 2017Review
- C-type lectin receptors in tuberculosis: what we know.Medical microbiology and immunology · 2016Review
- Association of Mannose-binding Lectin Polymorphisms with Tuberculosis Susceptibility among Chinese.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have demonstrated that mannose-binding lectin (MBL) recognizes various slow-growing, pathogenic mycobacteria [Mycobacterium tuberculosis (MTB), M. bovis, M. kansasii, M. gordonae] as well as non-pathogenic M. smegmatis. Recognition resulted in activation of the lectin pathway (LP) of complement and an enhancement of phagocytosis (shown for M. tuberculosis). Although MBL may be considered the main factor activating the LP upon recognition of mycobacteria, involvement of ficolins has also to be considered. Interaction of ficolin-3 with M. tuberculosis, M. bovis and M. kansasii, and ficolin-1 with M. tuberculosis and M. bovis was shown for the first time. Binding of recombinant MBL or ficolin-3 to MTB H37 Rv led to the agglutination of bacteria and promoted their phagocytosis, but little effect was apparent with ficolin-1 or ficolin-2. Data from Western blots suggest mannosylated lipoarabinomannan (ManLAM) to be one of the main cell components of slow-growing mycobacteria, involved in LP activation. However, the LP was also activated by other cell fractions. Results presented here supplement considerably the data concerning the ability of complement-activating lectins to interact with mycobacteria. Ficolins (especially ficolin-3) might influence host response to infection and thus have clinical significance, at least as disease modifiers.
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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.