ArticleScientific reports2018
IL-36/LXR axis modulates cholesterol metabolism and immune defense to Mycobacterium tuberculosis.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 48 citations in OpenAlex.
- IL-36γ enhanced bactericidal effects of macrophages to Mycobacterium tuberculosis via the IFN-γ/HIF-1ɑ/glycolysis pathway.Respiratory research · 2026Article
- Immunometabolic reprogramming ofFrontiers in tuberculosis · 2026Article
- Beyond VDR: Vitamin D Metabolism Genes in Tuberculosis Susceptibility, Immune Response and Implications for Diabetes Mellitus.Infection and drug resistance · 2026Review
- B cells inhibit IL-1 family cytokine production and Mycobacterium tuberculosis growth in human CD14+ cells.ImmunoHorizons · 2025Article
- Metabolic reprogramming of immune cells in the battle against intracellular bacterial chronic infections: novel mechanisms and breakthroughs.Molecular biology reports · 2025Review
- Advances in Host-Pathogen Interactions in Tuberculosis: Emerging Strategies for Therapeutic Intervention.International journal of molecular sciences · 2025Review
- Activation of nuclear receptors correlates with tuberculosis severity and is a target for host-directed therapy.Frontiers in cellular and infection microbiology · 2025Article
- Immune-endocrine crossroads: the impact of nuclear receptors in Tuberculosis and Chagas disease.Frontiers in endocrinology · 2025Review
- Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation.Cardiovascular research · 2024Article
- The role of cholesterol and its oxidation products in tuberculosis pathogenesis.Immunometabolism (Cobham, Surrey) · 2024Review
- Oxysterols in Infectious Diseases.Advances in experimental medicine and biology · 2024Article
- G9a and Sirtuin6 epigenetically modulate host cholesterol accumulation to facilitate mycobacterial survival.PLoS pathogens · 2023Article
- Revolutionizing control strategies against Mycobacterium tuberculosis infection through selected targeting of lipid metabolism.Cellular and molecular life sciences : CMLS · 2023Review
- Rifampicin drug resistance and host immunity in tuberculosis: more than meets the eye.Trends in immunology · 2023Review
- Host cell transcriptomic response to the multidrug-resistantVirulence · 2022Article
- Rapid GPR183-mediated recruitment of eosinophils to the lung after Mycobacterium tuberculosis infection.Cell reports · 2022Article
- Differential Modulation of Nuclear Receptor LRH-1 through Targeting Buried and Surface Regions of the Binding Pocket.Journal of medicinal chemistry · 2022Article
- Review
- PPARγ AmelioratesFrontiers in microbiology · 2022Article
- Compartmentalization of interleukin 36 subfamily according to inducible and constitutive expression in the kidneys of a murine autoimmune nephritis model.Cell and tissue research · 2021Article
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
Mycobacterium tuberculosis (Mtb) is a life-threatening pathogen in humans. Bacterial infection of macrophages usually triggers strong innate immune mechanisms, including IL-1 cytokine secretion. The newer member of the IL-1 family, IL-36, was recently shown to be involved in cellular defense against Mtb. To unveil the underlying mechanism of IL-36 induced antibacterial activity, we analyzed its role in the regulation of cholesterol metabolism, together with the involvement of Liver X Receptor (LXR) in this process. We report that, in Mtb-infected macrophages, IL-36 signaling modulates cholesterol biosynthesis and efflux via LXR. Moreover, IL-36 induces the expression of cholesterol-converting enzymes and the accumulation of LXR ligands, such as oxysterols. Ultimately, both IL-36 and LXR signaling play a role in the regulation of antimicrobial peptides expression and in Mtb growth restriction. These data provide novel evidence for the importance of IL-36 and cholesterol metabolism mediated by LXR in cellular host defense against Mtb.
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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.