ArticlePLoS pathogens2018
Mycobacterium tuberculosis-induced miR-155 subverts autophagy by targeting ATG3 in human dendritic cells.
Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.
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Who cites it
70 citing papers in PubMed, 129 citations in OpenAlex.
- Different MicroRNAs expression inRNA biology · 2026Review
- Epigenetic Reprogramming byAntibiotics (Basel, Switzerland) · 2026Review
- Functional analysis of distinct factors linked to the development of latent to active tuberculosis.Frontiers in cellular and infection microbiology · 2026Review
- Identification of apoptosis-related genes as potential biomarkers and therapeutic targets in cystic fibrosis patients progressing to pulmonary nontuberculous mycobacterial disease.Scientific reports · 2025Article
- ATG-3 limits Orsay virus infection in C. elegans and regulates collagen pathways.PLoS pathogens · 2025Article
- The pathway of autophagy in the epigenetic landscape ofAutophagy · 2025Review
- MicroRNAs in Liver Cirrhosis: Diagnostic and Therapeutic Perspectives-A Comprehensive Review.Journal of personalized medicine · 2025Review
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- Recent advances in the development and clinical application of miRNAs in infectious diseases.Non-coding RNA research · 2025Review
- Dysregulation of the JNK signaling pathway in tuberculosis: mechanisms and therapeutic strategies.Frontiers in cellular and infection microbiology · 2025Review
- Autophagy in mycobacterial infections: molecular mechanisms, host-pathogen interactions, and therapeutic opportunities.Frontiers in cellular and infection microbiology · 2025Review
- The Role of Deregulated MicroRNAs in Immune Cells of Sjögren's Disease.International journal of general medicine · 2025Review
- Epigenetic Mechanisms Induced byInternational journal of molecular sciences · 2024Review
- Non-Mutational Changes of Autophagy Marker LC3A in Patients with Acute Myeloid Leukemia; Effect of DNA Methylation and Expression Level of LncRNA-GAS5 and miRNA-155-5p, A Case Control Study.Indian journal of hematology & blood transfusion : an official journal of Indian Society of Hematology and Blood Transfusion · 2024Article
- Functional Analysis of Genes inIndian journal of microbiology · 2024Review
- Macrophage-derived extracellular vesicles fromFrontiers in immunology · 2024Article
- NCoR1 controls Mycobacterium tuberculosis growth in myeloid cells by regulating the AMPK-mTOR-TFEB axis.PLoS biology · 2023Article
- MicroRNAs as Biomarkers of Active Pulmonary TB Course.Microorganisms · 2023Article
- The role of miRNAs in Behçet's disease.Frontiers in immunology · 2023Review
10 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
15 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Autophagy is a primordial eukaryotic pathway, which provides the immune system with multiple mechanisms for the elimination of invading pathogens including Mycobacterium tuberculosis (Mtb). As a consequence, Mtb has evolved different strategies to hijack the autophagy process. Given the crucial role of human primary dendritic cells (DC) in host immunity control, we characterized Mtb-DC interplay by studying the contribution of cellular microRNAs (miRNAs) in the post-transcriptional regulation of autophagy related genes. From the expression profile of de-regulated miRNAs obtained in Mtb-infected human DC, we identified 7 miRNAs whose expression was previously found to be altered in specimens of TB patients. Among them, gene ontology analysis showed that miR-155, miR-155* and miR-146a target mRNAs with a significant enrichment in biological processes linked to autophagy. Interestingly, miR-155 was significantly stimulated by live and virulent Mtb and enriched in polysome-associated RNA fraction, where actively translated mRNAs reside. The putative pair interaction among the E2 conjugating enzyme involved in LC3-lipidation and autophagosome formation-ATG3-and miR-155 arose by target prediction analysis, was confirmed by both luciferase reporter assay and Atg3 immunoblotting analysis of miR-155-transfected DC, which showed also a consistent Atg3 protein and LC3 lipidated form reduction. Late in infection, when miR-155 expression peaked, both the level of Atg3 and the number of LC3 puncta per cell (autophagosomes) decreased dramatically. In accordance, miR-155 silencing rescued autophagosome number in Mtb infected DC and enhanced autolysosome fusion, thereby supporting a previously unidentified role of the miR-155 as inhibitor of ATG3 expression. Taken together, our findings suggest how Mtb can manipulate cellular miRNA expression to regulate Atg3 for its own survival, and highlight the importance to develop novel therapeutic strategies against tuberculosis that would boost autophagy.
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