ArticleInfection and immunity2010
Mycobacterium leprae actively modulates the cytokine response in naive human monocytes.
Article in Infection and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 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.
The trial behind it
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
22 citing papers in PubMed, 54 citations in OpenAlex.
- AMetabolites · 2026Article
- Leprosy: treatment, prevention, immune response and gene function.Frontiers in immunology · 2024Review
- A nod to the bond between NOD2 and mycobacteria.PLoS pathogens · 2023Review
- Allele-dependent interaction of LRRK2 and NOD2 in leprosy.PLoS pathogens · 2023Article
- Protective Efficacy of BCG Vaccine againstVaccines · 2022Review
- TLR-9 Plays a Role inFrontiers in immunology · 2021Article
- Organization of the Skin Immune System and Compartmentalized Immune Responses in Infectious Diseases.Clinical microbiology reviews · 2019Review
- The inflammasome in leprosy skin lesions: an immunohistochemical evaluation.Infection and drug resistance · 2018Article
- Type I Interferons, Autophagy and Host Metabolism in Leprosy.Frontiers in immunology · 2018Review
- Leprosy As a Complex Infection: Breakdown of the Th1 and Th2 Immune Paradigm in the Immunopathogenesis of the Disease.Frontiers in immunology · 2017Review
- Immune Checkpoints in Leprosy: Immunotherapy As a Feasible Approach to Control Disease Progression.Frontiers in immunology · 2017Article
- Mycobacterium leprae-induced Insulin-like Growth Factor I attenuates antimicrobial mechanisms, promoting bacterial survival in macrophages.Scientific reports · 2016Article
- Genetic Variation in Toll-Interacting Protein Is Associated With Leprosy Susceptibility and Cutaneous Expression of Interleukin 1 Receptor Antagonist.The Journal of infectious diseases · 2016Article
- Mycobacterium leprae alters classical activation of human monocytes in vitro.Journal of inflammation (London, England) · 2016Article
- Virulent Type A Francisella tularensis actively suppresses cytokine responses in human monocytes.Frontiers in cellular and infection microbiology · 2014Article
- NFκB activation in cutaneous lesions of leprosy is associated with development of multibacillary infection.Journal of inflammation research · 2014Article
- Article
- Gene expression profiling specifies chemokine, mitochondrial and lipid metabolism signatures in leprosy.PloS one · 2013Article
- PARK2 mediates interleukin 6 and monocyte chemoattractant protein 1 production by human macrophages.PLoS neglected tropical diseases · 2013Article
- MicroRNA-21 targets the vitamin D-dependent antimicrobial pathway in leprosy.Nature medicine · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Leprosy is a chronic but treatable infectious disease caused by the intracellular pathogen Mycobacterium leprae. Host immunity to M. leprae determines the diversity of clinical manifestations seen in patients, from tuberculoid leprosy with robust production of Th1-type cytokines to lepromatous disease, characterized by elevated levels of Th2-type cytokines and a suboptimal proinflammatory response. Previous reports have indicated that M. leprae is a poor activator of macrophages and dendritic cells in vitro. To understand whether M. leprae fails to elicit an optimal Th1 immune response or actively interferes with its induction, we have examined the early interactions between M. leprae and monocytes from healthy human donors. We found that, in naïve monocytes, M. leprae induced high levels of the negative regulatory molecules MCP-1 and interleukin-1 (IL-1) receptor antagonist (IL-1Ra), while suppressing IL-6 production through phosphoinositide-3 kinase (PI3K)-dependent mechanisms. In addition, low levels of proinflammatory cytokines were observed in association with reduced activation of nuclear factor-kappaB (NF-kappaB) and delayed activation of IL-1beta-converting enzyme, ICE (caspase-1), in monocytes stimulated with M. leprae compared with Mycobacterium bovis BCG stimulation. Interestingly, although in itself a weak stimulator of cytokines, M. leprae primed the cells for increased production of tumor necrosis factor alpha and IL-10 in response to a strongly inducing secondary stimulus. Taken together, our results suggest that M. leprae plays an active role to control the release of cytokines from monocytes by providing both positive and negative regulatory signals via multiple signaling pathways involving PI3K, NF-kappaB, and caspase-1.
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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.