ReviewFrontiers in immunology2014
Reverse translation in tuberculosis: neutrophils provide clues for understanding development of active disease.
Review in Frontiers in immunology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
17 citing papers in PubMed.
- Identification of a Four-Biomarker Panel for the Diagnosis of Tuberculous Pleural Effusion Using Olink Proteomics.Journal of inflammation research · 2026Article
- Type I interferons in bacterial diseases: myeloid cells at the crossroads of protection and pathology.Frontiers in immunology · 2025Review
- Article
- miR-223: a key regulator of pulmonary inflammation.Frontiers in medicine · 2023Review
- Differential Role of Type 2 Diabetes as a Risk Factor for Tuberculosis in the Elderly versus Younger Adults.Pathogens (Basel, Switzerland) · 2022Article
- MicroRNAs as immune regulators and biomarkers in tuberculosis.Frontiers in immunology · 2022Review
- Immunological roulette: Luck or something more? Considering the connections between host and environment in TB.Cellular & molecular immunology · 2018Review
- Host-directed therapies for bacterial and viral infections.Nature reviews. Drug discovery · 2018Review
- Article
- Innate myeloid cell TNFR1 mediates first line defence against primary Mycobacterium tuberculosis infection.Scientific reports · 2016Article
- Protection and pathology in TB: learning from the zebrafish model.Seminars in immunopathology · 2016Review
- Neutrophil Extracellular Traps in Pulmonary Diseases: Too Much of a Good Thing?Frontiers in immunology · 2016Review
- Granulomas and Inflammation: Host-Directed Therapies for Tuberculosis.Frontiers in immunology · 2016Review
- Innate and Adaptive Cellular Immune Responses to Mycobacterium tuberculosis Infection.Cold Spring Harbor perspectives in medicine · 2015Review
- The human immune response to tuberculosis and its treatment: a view from the blood.Immunological reviews · 2015Review
- Identifcation of differentially expressed long non-coding RNAs in CD4+ T cells response to latent tuberculosis infection.The Journal of infection · 2014Article
- Striking the Right Balance Determines TB or Not TB.Frontiers in immunology · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Tuberculosis (TB) is a major health issue globally. Although typically the disease can be cured by chemotherapy in all age groups, and prevented in part in newborn by vaccination, general consensus exists that development of novel intervention measures requires better understanding of disease mechanisms. Human TB is characterized by polarity between host resistance as seen in 2 billion individuals with latent TB infection and susceptibility occurring in 9 million individuals who develop active TB disease every year. Experimental animal models often do not reflect this polarity adequately, calling for a reverse translational approach. Gene expression profiling has allowed identification of biomarkers that discriminate between latent infection and active disease. Functional analysis of most relevant markers in experimental animal models can help to better understand mechanisms driving disease progression. We have embarked on in-depth characterization of candidate markers of pathology and protection hereby harnessing mouse mutants with defined gene deficiencies. Analysis of mutants deficient in miR-223 expression and CXCL5 production allowed elucidation of relevant pathogenic mechanisms. Intriguingly, these deficiencies were linked to aberrant neutrophil activities. Our findings point to a detrimental potential of neutrophils in TB. Reciprocally, measures that control neutrophils should be leveraged for amelioration of TB in adjunct to chemotherapy.
Indexed as
Identifiers
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.