miRNAs in immune responses to Mycobacterium tuberculosis infection
Abstract
Tuberculosis (TB) is one of the most fatal infectious diseases, affecting one third of the world's population. The causative agent, Mycobacterium tuberculosis (Mtb), has a well-established ability to circumvent the host's immune system for its long-term intracellular survival. MicroRNAs (miRNAs) are crucial post-transcriptional regulators of immune response. They act by negatively regulating the expression levels of important genes in both innate and adaptive immunity. It has been established in recent studies that the host immune response against Mtb is regulated by many miRNAs, most of which are induced by Mtb infection. Moreover, differential expression of miRNA in tuberculosis (TB) patients may help distinguish between TB patients and healthy individuals or latent TB. In this review, we present the recent advancements on the miRNA regulation of the host responses against Mtb infection, as well as the potential of miRNAs to as biomarkers for TB diagnosis.
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During Mtb infection, miR-26a is downregulated, leading to upregulation of KLF4 and stimulation of the M2 phenotype.
“Interestingly, during Mtb infection, miR-26a is downregulated, leading to upregulation of KLF4 and stimulation of the M2 phenotype [198].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [198]
A negative correlation between miR-142-3p activity and Mtb internalization is caused by targeting PKCα.
“A negative correlation of miR-142–3p activity and Mtb internalization was caused by targeting PKC alpha, a key regulator involved in phagocytosis [198].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [198]
miR-142-3p targets N-wasp, an actin-binding protein regulating actin dynamics during bacterial uptake.
“miR-142–3p targets N-wasp, an actin-binding protein regulating actin dynamics during bacterial uptake [145,198].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [198]
miR-106-5p is upregulated by Mtb infection in macrophages and targets cathepsin S mRNA, decreasing lysosomal activity.
“miR-106-5p, a microRNA upregulated by Mtb infection in macrophages and targets cathepsin S (CtsS) mRNA, thus decreasing lysosomal activity [136,198].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [198]
miR-582-5p and miR-223 inhibit apoptosis by suppressing FOXO1 and FOXO3, and let-7b-5p targets the 3′-UTR of Fas.
“miR-582-5p and miR-223 inhibited apoptosis by suppression FOXO1 and FOXO3. In turn, let-7b-5p has been identified as a microRNA targeting the 3′-UTR of Fas, a protein with a central role in the regulation of apoptosis [198].”
From MicroRNAs as Regulators of Phagocytosis (2022) · cites this paper as [198]
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- Authors
- Yang, T., & Ge, B.
- Affiliations
- Tongji University (CN)
- Corresponding author
- Ge, Baoxue
- Venue
- Cancer Letters
- Publisher
- Elsevier BV
- Published
- 2018-09
- Volume
- 431
- Pages
- 22-30
- ISSN
- 0304-3835 (ISSN-L)
- OpenAlex
- W2803132334
- Cited by
- 78
- References
- 125
- Citations by year
- 2026: 4 · 2025: 11 · 2024: 7 · 2023: 11 · 2022: 13 · 2021: 14 · 2020: 10 · 2019: 5 · 2018: 3
- FWCI
- 1.17
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Cancer Letters (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Program on Key Basic Research Project (2017YFA0505900, 2015CB964601)
- National Natural Science Foundation of China (91542111, 81330069, 31730025)
- Topics
- Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Health Sciences › Medicine › Surgery › Infectious Diseases and Tuberculosis
- Keywords
- microRNA, Mycobacterium tuberculosis, tuberculosis, host immune response, innate immunity, adaptive immunity, post-transcriptional regulation, microRNA biomarkers, tuberculosis diagnosis, latent tuberculosis infection, intracellular survival
- MeSH terms
- Autophagy, Dendritic Cells, Humans, Immune System, Immunity, Innate, Macrophages, Mycobacterium tuberculosis, Phagocytosis, Polymorphism, Genetic, Tuberculosis, Signal Transduction, Biomarkers, Gene Expression Regulation, Bacterial, Genetic Predisposition to Disease, MicroRNAs, Adaptive Immunity
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