ArticleEBioMedicine2017
IL-17 Production of Neutrophils Enhances Antibacteria Ability but Promotes Arthritis Development During Mycobacterium tuberculosis Infection.
Article in EBioMedicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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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Who cites it
42 citing papers in PubMed, 69 citations in OpenAlex.
- Context-specific roles for IL-17 in tuberculosis.PLoS pathogens · 2026Review
- Article
- MAPK signaling pathways in host immune regulation during Mycobacterium tuberculosis infection.Frontiers in immunology · 2026Review
- Calreticulin in the nasal mucus promotes neutrophil migration and pathogen clearance.Cell communication and signaling : CCS · 2025Article
- Kurarinone regulates Th17/Treg balance and ameliorates autoimmune uveitis via Rac1 inhibition.Journal of advanced research · 2025Article
- Implications for neutrophils in cardiac arrhythmias.American journal of physiology. Heart and circulatory physiology · 2024Review
- IL-27 alters inflammatory cytokine expression and limits protective immunity againstFrontiers in immunology · 2024Article
- How Neutrophils Shape the Immune Response: Reassessing Their Multifaceted Role in Health and Disease.International journal of molecular sciences · 2023Review
- Autophagy prevents early proinflammatory responses and neutrophil recruitment during Mycobacterium tuberculosis infection without affecting pathogen burden in macrophages.PLoS biology · 2023Article
- Neutrophil-derived interleukin-17A participates in neuroinflammation induced by traumatic brain injury.Neural regeneration research · 2023Article
- Role of phagocyte extracellular traps duringFrontiers in microbiology · 2023Review
- Attenuation of relapsing fever neuroborreliosis in mice by IL-17A blockade.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Helminth species dependent effects on Th1 and Th17 cytokines in active tuberculosis patients and healthy community controls.PLoS neglected tropical diseases · 2022Article
- The Protective Role of pVHL in Imiquimod-Induced Psoriasis-like Skin Inflammation.International journal of molecular sciences · 2022Article
- It Takes a Village: The Multifaceted Immune Response toFrontiers in immunology · 2022Review
- E, K, B5, B6, and B9 vitamins and their specific immunological effects evaluated by flow cytometry.Frontiers in medicine · 2022Review
- IL-17RA receptor signaling contributes to lung inflammation and parasite burden duringFrontiers in immunology · 2022Article
- Hyperinflammatory environment drives dysfunctional myeloid cell effector response to bacterial challenge in COVID-19.PLoS pathogens · 2022Article
- Immunological Assessment of Chitosan or Trimethyl Chitosan-Coated PLGA Nanospheres Containing Fusion Antigen as the Novel Vaccine Candidates Against Tuberculosis.AAPS PharmSciTech · 2021Article
- IL-17A reprograms intestinal epithelial cells to facilitate HIV-1 replication and outgrowth in CD4+ T cells.iScience · 2021Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
To our knowledge, no studies have examined the role of IL-17 production by neutrophils in immune defense against Mycobacterium tuberculosis (MTB) infection and the pathogenesis of rheumatoid arthritis (RA) caused by MTB infection. Here, we determined that neutrophils express IL-17 in an autocrine IL-6- and IL-23-dependent manner during MTB infection. MTB H37Rv-induced IL-6 production was dependent on the NF-κB, p38, and JNK signaling pathways; however, IL-23 production was dependent on NF-κB and EKR in neutrophils. Furthermore, we found that Toll-like receptor 2 (TLR2) and TLR4 mediated the activation of the kinases NF-κB, p38, ERK, and JNK and the production of IL-6, IL-23, and IL-17 in neutrophils infected with MTB H37Rv. Autocrine IL-17 produced by neutrophils played a vital role in inhibiting MTB H37Rv growth by mediating reactive oxygen species production and the migration of neutrophils in the early stages of infection. However, IL-17 production by neutrophils contributed to collagen-induced arthritis development during MTB infection. Our findings identify a protective mechanism against mycobacteria and the pathogenic role of MTB in arthritis development.
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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.