ReviewImmunological reviews2021
Reduction of host cell mitochondrial activity as Mycobacterium leprae's strategy to evade host innate immunity.
Review in Immunological reviews, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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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
19 citing papers in PubMed, 23 citations in OpenAlex.
- AMetabolites · 2026Article
- Mitochondria in SARS-CoV-2 infection: Immune interactions and molecular approaches in the Post COVID-19 condition.Genetics and molecular biology · 2026Article
- Article
- Pathologic and Therapeutic Schwann Cells.Cells · 2025Review
- Schwann cells in regeneration and cancer: an epithelial-mesenchymal transition perspective.Open biology · 2025Review
- The research progress of LACC1.Frontiers in immunology · 2025Review
- Gene expression profiling in pure neural leprosy: insights into pathogenesis and diagnostic biomarkers.Frontiers in immunology · 2025Article
- High-Resolution Plasma Metabolomics Identifies Alterations in Fatty Acid, Energy, and Micronutrient Metabolism in Adults Across the Leprosy Spectrum.The Journal of infectious diseases · 2024Article
- MicroRNA biomarkers in leprosy: insights from the Northern Brazilian Amazon population and their implications in disease immune-physiopathology.Frontiers in genetics · 2024Article
- Whole mitogenome sequencing uncovers a relation between mitochondrial heteroplasmy and leprosy severity.Human genomics · 2023Article
- Mitochondrial Dysfunction in Bacterial Infections.Pathogens (Basel, Switzerland) · 2023Review
- Evidencing leprosy neuronal inflammation by 18-Fluoro-deoxy-glucose.PLoS neglected tropical diseases · 2023Article
- Mitochondria inInternational journal of molecular sciences · 2022Review
- Kynurenines in the Pathogenesis of Peripheral Neuropathy During Leprosy and COVID-19.Frontiers in cellular and infection microbiology · 2022Review
- Article
- Modulation of the Response toFrontiers in microbiology · 2022Review
- Gene Expression Profile ofFrontiers in medicine · 2022Article
- Derivation and Clinical Validation of a Redox-Driven Prognostic Signature for Colorectal Cancer.Frontiers in oncology · 2021Article
- Host Immune-Metabolic Adaptations Upon Mycobacterial Infections and Associated Co-Morbidities.Frontiers in immunology · 2021Review
Corrections and comments
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Authors and funding
15 authors at 3 institutions in 1 country.
Funding
Abstract
Leprosy is a much-feared incapacitating infectious disease caused by Mycobacterium leprae or M lepromatosis, annually affecting roughly 200,000 people worldwide. During host-pathogen interaction, M leprae subverts the immune response, leading to development of disease. Throughout the last few decades, the impact of energy metabolism on the control of intracellular pathogens and leukocytic differentiation has become more evident. Mitochondria play a key role in regulating newly-discovered immune signaling pathways by controlling redox metabolism and the flow of energy besides activating inflammasome, xenophagy, and apoptosis. Likewise, this organelle, whose origin is probably an alphaproteobacterium, directly controls the intracellular pathogens attempting to invade its niche, a feature conquered at the expense of billions of years of coevolution. In the present review, we discuss the role of reduced host cell mitochondrial activity during M leprae infection and the consequential fates of M leprae and host innate immunity. Conceivably, inhibition of mitochondrial energy metabolism emerges as an overlooked and novel mechanism developed by M leprae to evade xenophagy and the host immune response.
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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.