ArticlePloS one2011
CCL2/MCP-I genotype-phenotype relationship in latent tuberculosis infection.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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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
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 35 citations in OpenAlex.
- The role of host genetic factors in respiratory tract infectious diseases: systematic review, meta-analyses and field synopsis.Scientific reports · 2015Pooled it
- Genetic association meta-analysis: a new classification to assess ethnicity using the association of MCP-1 -2518 polymorphism and tuberculosis susceptibility as a model.BMC genetics · 2015Pooled it
- Article
- Effect of PPD inoculation on serum cytokine profiles in latent tuberculosis infection populations.Frontiers in cellular and infection microbiology · 2025Article
- Insights intoProteomes · 2021Review
- Coexistent Helminth Infection-Mediated Modulation of Chemokine Responses in Latent Tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2019Article
- Immune-related gene polymorphisms in pulmonary diseases.Toxicology · 2017Review
- Low Dose BCG Infection as a Model for Macrophage Activation Maintaining Cell Viability.Journal of immunology research · 2016Article
- The role of chemokine C-C motif ligand 2 genotype and cerebrospinal fluid chemokine C-C motif ligand 2 in neurocognition among HIV-infected patients.AIDS (London, England) · 2015Article
- Ebola: translational science considerations.Journal of translational medicine · 2015Review
- Article
- IP-10 and MIG are compartmentalized at the site of disease during pleural and meningeal tuberculosis and are decreased after antituberculosis treatment.Clinical and vaccine immunology : CVI · 2014Article
- Latent tuberculosis infection: myths, models, and molecular mechanisms.Microbiology and molecular biology reviews : MMBR · 2014Review
- The involvement of NADPH oxidase-mediated ROS in cytokine secretion from macrophages induced by Mycobacterium tuberculosis ESAT-6.Inflammation · 2014Article
- Identification of biomarkers for tuberculosis susceptibility via integrated analysis of gene expression and longitudinal clinical data.Frontiers in genetics · 2014Article
- Classical and alternative macrophage activation in the lung following ozone-induced oxidative stress.Toxicology and applied pharmacology · 2012Article
- New biomarkers with relevance to leprosy diagnosis applicable in areas hyperendemic for leprosy.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Cellular and humoral mechanisms involved in the control of tuberculosis.Clinical & developmental immunology · 2012Review
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
Among the known biomarkers, chemokines, secreted by activated macrophages and T cells, attract groups of immune cells to the site of infection and may determine the clinical outcome. Association studies of CCL-2/MCP-1 -2518 A/G functional SNP linked to high and low phenotypes with tuberculosis disease susceptibility have shown conflicting results in tuberculosis. Some of these differences could be due the variability of latent infection and recent exposure in the control groups. We have therefore carried out a detailed analysis of CCL-2 genotype SNP -2518 (A/G transition) with plasma CCL-2 levels and related these levels to tuberculin skin test positivity in asymptomatic community controls with no known exposure to tuberculosis and in recently exposed household contacts of pulmonary tuberculosis patients. TST positivity was linked to higher concentrations of plasma CCL2 (Mann Whitney U test; p = 0.004) and was more marked when the G allele was present in TST+ asymptomatic controls (A/G; p = 0.01). Recent exposure also had a significant effect on CCL-2 levels and was linked to the G allele (p = 0.007). Therefore association studies for susceptibility or protection from disease should take into consideration the PPD status as well as recent exposure of the controls group used for comparison. Our results also suggest a role for CCL-2 in maintaining the integrity of granuloma in asymptomatic individuals with latent infection in high TB burden settings. Therefore additional studies into the role of CCL-2 in disease reactivation and progression are warranted.
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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.