ArticleNature2013
Temperature triggers immune evasion by Neisseria meningitidis.
Article in Nature, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 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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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
74 citing papers in PubMed, 148 citations in OpenAlex.
- Emergence of short-lived meningococci causing focal epidemics can be associated with gene transfer from carriage-associatedbioRxiv : the preprint server for biology · 2026Article
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- Mechanisms of thermoregulation inJournal of bacteriology · 2026Review
- Article
- Genotypic and phenotypic comparison of Neisseria meningitidis carriage and invasive disease isolates contemporaneously collected in the Netherlands.FEMS microbiology letters · 2026Article
- The cycle of infectious fever - how it affects bacterial infections.Frontiers in cellular and infection microbiology · 2026Review
- Exploring the sequence diversity and surface expression of Factor H-Binding Protein among invasive serogroup B meningococcal strains from selected European countries.Human vaccines & immunotherapeutics · 2024Article
- Universal cold RNA phase transitions.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Determinants of bacterial survival and proliferation in blood.FEMS microbiology reviews · 2024Review
- Distributed genotyping and clustering of Neisseria strains reveal continual emergence of epidemic meningococcus over a century.Nature communications · 2023Article
- Meningococcal factor H-binding protein: implications for disease susceptibility, virulence, and vaccines.Trends in microbiology · 2023Review
- Developing New Tools to Fight Human Pathogens: A Journey through the Advances in RNA Technologies.Microorganisms · 2022Review
- Neisseria genes required for persistence identified via in vivo screening of a transposon mutant library.PLoS pathogens · 2022Article
- Multilayer Regulation ofMicroorganisms · 2022Article
- The Host-Pathogen Interactions and Epicellular Lifestyle ofFrontiers in cellular and infection microbiology · 2022Review
- Genomic Insights on Variation Underlying Capsule Expression in Meningococcal Carriage Isolates From University Students, United States, 2015-2016.Frontiers in microbiology · 2022Article
- Low Levels of Factor H Family Proteins During Meningococcal Disease Indicate Systemic Processes Rather Than Specific Depletion byFrontiers in immunology · 2022Article
- The gatekeeper of Yersinia type III secretion is under RNA thermometer control.PLoS pathogens · 2021Article
- Genome-wide association studies reveal the role of polymorphisms affecting factor H binding protein expression in host invasion by Neisseria meningitidis.PLoS pathogens · 2021Article
- Lactate-Induced Dispersal ofInfection and immunity · 2021Article
14 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Neisseria meningitidis has several strategies to evade complement-mediated killing, and these contribute to its ability to cause septicaemic disease and meningitis. However, the meningococcus is primarily an obligate commensal of the human nasopharynx, and it is unclear why the bacterium has evolved exquisite mechanisms to avoid host immunity. Here we demonstrate that mechanisms of meningococcal immune evasion and resistance against complement increase in response to an increase in ambient temperature. We have identified three independent RNA thermosensors located in the 5' untranslated regions of genes necessary for capsule biosynthesis, the expression of factor H binding protein, and sialylation of lipopolysaccharide, which are essential for meningococcal resistance against immune killing. Therefore increased temperature (which occurs during inflammation) acts as a 'danger signal' for the meningococcus, enhancing its defence against human immune killing. Infection with viral pathogens, such as influenza, leads to inflammation in the nasopharynx with an increased temperature and recruitment of immune effectors. Thermoregulation of immune defence could offer an adaptive advantage to the meningococcus during co-infection with other pathogens, and promote the emergence of virulence in an otherwise commensal bacterium.
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What OpenQuestion holds
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.