ArticlePloS one2016
Overexpression of RORγt Enhances Pulmonary Inflammation after Infection with Mycobacterium Avium.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 14 citations in OpenAlex.
- RORγt Mediates Angiotensin II-Induced Pressor Responses, Microglia Activation, and Neuroinflammation by Disrupting the Blood-Brain Barrier in Rats.Journal of the American Heart Association · 2025Article
- A novel loss-of-function variant inFrontiers in cellular and infection microbiology · 2025Article
- Vaccination inducing durable and robust antigen-specific Th1/Th17 immune responses contributes to prophylactic protection againstVirulence · 2022Article
- DNA Methylation Profiling for the Diagnosis and Prognosis of Patients with NontuberculousCurrent issues in molecular biology · 2021Article
- Antimicrobial Activity of Neutrophils Against Mycobacteria.Frontiers in immunology · 2021Review
- Esculetin Ameliorates Lipopolysaccharide-Induced Acute Lung Injury in Mice Via Modulation of the AKT/ERK/NF-κB and RORγt/IL-17 Pathways.Inflammation · 2020Article
- Article
- The Rise of Non-Tuberculosis Mycobacterial Lung Disease.Frontiers in immunology · 2020Review
- Elevated maternal retinoic acid-related orphan receptor-γt enhances the effect of polyinosinic-polycytidylic acid in inducing fetal loss.Experimental animals · 2019Article
- Molecular dynamics simulations on RORγt: insights into its functional agonism and inverse agonism.Acta pharmacologica Sinica · 2019Article
- Toll Like Receptor 4 Mediated Lymphocyte Imbalance Induces Nec-Induced Lung Injury.Shock (Augusta, Ga.) · 2019Article
- Transcriptional Response of Respiratory Epithelium to Nontuberculous Mycobacteria.American journal of respiratory cell and molecular biology · 2018Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium avium complex (MAC) is the most common cause of nontuberculous mycobacterial disease in humans. The role of Th17 immunity in the pathogenesis of intracellular bacteria, such as MAC, is not currently understood. Transcription factor RAR-related orphan receptor gamma t (RORγt) is known as the master regulator for Th17 cell development. Here, we investigated the role of RORγt in host responses against MAC infection. Wild-type (WT) mice and RORγt-overexpressing mice were infected with MAC via intratracheal inoculation. Systemic MAC growth was not different between WT mice and RORγt-overexpressing mice. However, neutrophilic pulmonary inflammation following MAC infection was enhanced in RORγt-overexpressing mice compared with that in WT mice. The cytokine expression shifted toward a Th17 phenotype in the lungs of RORγt-overexpressing mice following MAC infection; the levels of IL-6 and IL-17 were significantly higher in the lung of these mice than in WT mice. In addition to the increase in IL-17 single-positive T cells, T cells producing both IL-17 and interferon-γ were elevated in the lung of RORγt-overexpressing mice following MAC infection. These findings suggest that RORγt overexpression-mediated Th17 bias contributes to local inflammation rather than systemic responses, by regulating neutrophil recruitment into the sites of infection during MAC infection.
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