ArticleImmunology2015
Microarray analysis of Mycobacterium tuberculosis-infected monocytes reveals IL26 as a new candidate gene for tuberculosis susceptibility.
Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Multifaceted Roles of IL-26 in Physiological and Pathological Conditions.International journal of molecular sciences · 2025Review
- The evolving landscape of IL-10, IL-22 and IL-26 in pleurisy especially in tuberculous pleurisy.Respiratory research · 2024Review
- The Diverse Roles of Monocytes in Cryptococcosis.Journal of fungi (Basel, Switzerland) · 2020Review
- Interleukin-26 is overexpressed in human sepsis and contributes to inflammation, organ injury, and mortality in murine sepsis.Critical care (London, England) · 2019Article
- Interleukin-26 upregulates interleukin-22 production by human CD4Journal of molecular medicine (Berlin, Germany) · 2019Article
- IL-26 contributes to host defense against intracellular bacteria.The Journal of clinical investigation · 2019Article
- IL-26, a Cytokine With Roles in Extracellular DNA-Induced Inflammation and Microbial Defense.Frontiers in immunology · 2019Review
- Identification and Classification of Differentially Expressed Genes and Network Meta-Analysis Reveals Potential Molecular Signatures Associated With Tuberculosis.Frontiers in genetics · 2019Article
- Interleukin-26 promotes the proliferation and activation of hepatic stellate cells to exacerbate liver fibrosis by the TGF-β1/Smad2 signaling pathway.International journal of clinical and experimental pathology · 2019Article
- Th1 cytokines, true functional signatures for protective immunity against TB?Cellular & molecular immunology · 2018Review
- Genetic Resistance toFrontiers in immunology · 2018Review
- Monocyte Subsets: Phenotypes and Function in Tuberculosis Infection.Frontiers in immunology · 2018Review
- Identification potential biomarkers in pulmonary tuberculosis and latent infection based on bioinformatics analysis.BMC infectious diseases · 2016Article
- Interleukin-10 Family and Tuberculosis: An Old Story Renewed.International journal of biological sciences · 2016Review
- Interleukin-26: An Emerging Player in Host Defense and Inflammation.Journal of innate immunity · 2016Review
- IL12, IL10, IFNγ and TNFα Expression in Human Primary Monocytes Stimulated with Bacterial Heat Shock GroEL (Hsp64) Protein.PloS one · 2016Article
- Cytokine and Antibody Based Diagnostic Algorithms for Sputum Culture-Positive Pulmonary Tuberculosis.PloS one · 2015Article
- Analysis of the Bovine Monocyte-Derived Macrophage Response to Mycobacterium avium Subspecies Paratuberculosis Infection Using RNA-seq.Frontiers in immunology · 2015Article
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
Differences in the activity of monocytes/macrophages, important target cells of Mycobacterium tuberculosis, might influence tuberculosis progression. With the purpose of identifying candidate genes for tuberculosis susceptibility we infected monocytes from both healthy elderly individuals (a tuberculosis susceptibility group) and elderly tuberculosis patients with M. tuberculosis, and performed a microarray experiment. We detected 78 differentially expressed transcripts and confirmed these results by quantitative PCR of selected genes. We found that monocytes from tuberculosis patients showed similar expression patterns for these genes, regardless of whether they were obtained from younger or older patients. Only one of the detected genes corresponded to a cytokine: IL26, a member of the interleukin-10 (IL-10) cytokine family which we found to be down-regulated in infected monocytes from tuberculosis patients. Non-infected monocytes secreted IL-26 constitutively but they reacted strongly to M. tuberculosis infection by decreasing IL-26 production. Furthermore, IL-26 serum concentrations appeared to be lower in the tuberculosis patients. When whole blood was infected, IL-26 inhibited the observed pathogen-killing capability. Although lymphocytes expressed IL26R, the receptor mRNA was not detected in either monocytes or neutrophils, suggesting that the inhibition of anti-mycobacterial activity may be mediated by lymphocytes. Additionally, IL-2 concentrations in infected blood were lower in the presence of IL-26. The negative influence of IL-26 on the anti-mycobacterial activity and its constitutive presence in both serum and monocyte supernatants prompt us to propose IL26 as a candidate gene for tuberculosis susceptibility.
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