ArticleThe Journal of clinical investigation2019
IL-26 contributes to host defense against intracellular bacteria.
Article in The Journal of clinical investigation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 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
36 citing papers in PubMed, 60 citations in OpenAlex.
- Identification of a spatially organized TREM2-associated permissive macrophage niche in human pulmonary tuberculosis alveolar pneumonia.Nature communications · 2026Article
- Cytokine multimerization: when more is more and sometimes less.Nature reviews. Immunology · 2026Review
- Gastrointestinal MAIT cells in chronic HIV-1 infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Pharmacological and genetic modulation of IL-32 expression in intestinal epithelial cells does not impact HIV-1 outgrowth in co-cultured CD4Frontiers in immunology · 2026Article
- T cell-macrophage interactions in tuberculosis: What we've got here is failure to communicate.Journal of internal medicine · 2026Review
- Article
- Dynamics of Th1/Th17 responses and antimicrobial pathways in leprosy skin lesions.The Journal of clinical investigation · 2025Article
- STING directly interacts with PAR to promote apoptosis upon acute ionizing radiation-mediated DNA damage.Cell death and differentiation · 2025Article
- Inducible antibacterial responses in macrophages.Nature reviews. Immunology · 2025Review
- Advancing Phage Therapy: A Comprehensive Review of the Safety, Efficacy, and Future Prospects for the Targeted Treatment of Bacterial Infections.Infectious disease reports · 2024Review
- Human neutrophils drive skin autoinflammation by releasing interleukin (IL)-26.The Journal of experimental medicine · 2024Article
- Interleukin-26 expression in tuberculosis disease and its regulatory effect in macrophage polarization and intracellular elimination ofFrontiers in cellular and infection microbiology · 2024Article
- Xenophagy as a Strategy forPathogens (Basel, Switzerland) · 2023Review
- A half-century of research on tuberculosis: Successes and challenges.The Journal of experimental medicine · 2023Article
- CD30 co-stimulation drives differentiation of protective T cells during Mycobacterium tuberculosis infection.The Journal of experimental medicine · 2023Article
- Th17 Cells and Cytokines in Leprosy: Understanding the Immune Response and Polarization.Revista da Sociedade Brasileira de Medicina Tropical · 2023Review
- Human lung-resident mucosal-associated invariant T cells are abundant, express antimicrobial proteins, and are cytokine responsive.Communications biology · 2022Article
- Interleukin-26 Expression in Inflammatory Bowel Disease and Its Immunoregulatory Effects on Macrophages.Frontiers in medicine · 2022Article
- The Missing Link in Correlates of Protective Tuberculosis Immunity: Recognizing the Infected Cell.Frontiers in immunology · 2022Review
- Interleukin-26-DNA complexes promote inflammation and dermal-epidermal separation in a modified human cryosection model of bullous pemphigoid.Frontiers in immunology · 2022Article
Corrections and comments
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Authors and funding
10 authors at 5 institutions in 3 countries.
Funding
Abstract
IL-26 is an antimicrobial protein secreted by Th17 cells that has the ability to directly kill extracellular bacteria. To ascertain whether IL-26 contributes to host defense against intracellular bacteria, we studied leprosy, caused by the obligate intracellular pathogen Mycobacterium leprae, as a model. Analysis of leprosy skin lesions by gene expression profiling and immunohistology revealed that IL-26 was more strongly expressed in lesions from the self-limited tuberculoid compared with expression in progressive lepromatous patients. IL-26 directly bound to M. leprae in axenic culture and reduced bacteria viability. Furthermore, IL-26, when added to human monocyte-derived macrophages infected with M. leprae, entered the infected cell, colocalized with the bacterium, and reduced bacteria viability. In addition, IL-26 induced autophagy via the cytoplasmic DNA receptor stimulator of IFN genes (STING), as well as fusion of phagosomes containing bacilli with lysosomal compartments. Altogether, our data suggest that the Th17 cytokine IL-26 contributes to host defense against intracellular bacteria.
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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.