ArticleImmunology2010
Toll-like receptor 6 drives interleukin-17A expression during experimental hypersensitivity pneumonitis.
Article in Immunology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 31 citations in OpenAlex.
- How experimental models have unlocked hidden mechanisms of hypersensitivity pneumonitis.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Biomarkers associated with immune-related adverse events induced by immune checkpoint inhibitors.World journal of clinical oncology · 2024Review
- Protein kinase D1 in myeloid lineage cells contributes to the accumulation of CXCR3Frontiers in immunology · 2024Article
- Diagnosis of Fibrotic Hypersensitivity Pneumonitis: Is There a Role for Biomarkers?Life (Basel, Switzerland) · 2023Review
- Cytokine changes during immune-related adverse events and corticosteroid treatment in melanoma patients receiving immune checkpoint inhibitors.Cancer immunology, immunotherapy : CII · 2021Article
- S1PAmerican journal of respiratory cell and molecular biology · 2020Article
- Hypersensitivity pneumonitis onset and severity is regulated by CD103 dendritic cell expression.PloS one · 2017Article
- Chronic hypersensitivity pneumonitis caused by Saccharopolyspora rectivirgula is not associated with a switch to a Th2 response.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- A critical role of Dectin-1 in hypersensitivity pneumonitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2016Article
- Toll-like receptor 6 stimulation promotes T-helper 1 and 17 responses in gastrointestinal-associated lymphoid tissue and modulates murine experimental colitis.Mucosal immunology · 2014Article
- Management of hypersensivity pneumonitis.Clinical and translational allergy · 2013Article
- TLR2 regulates neutrophil recruitment and cytokine production with minor contributions from TLR9 during hypersensitivity pneumonitis.PloS one · 2013Article
- TLR9-dependent IL-23/IL-17 is required for the generation of Stachybotrys chartarum-induced hypersensitivity pneumonitis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Stachybotrys chartarum-induced hypersensitivity pneumonitis is TLR9 dependent.The American journal of pathology · 2011Article
- Toll like receptors in diseases of the lung.International immunopharmacology · 2011Review
- Innate immunity and the pathogenicity of inhaled microbial particles.International journal of biological sciences · 2011Review
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 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hypersensitivity pneumonitis (HP) is a T-cell-driven disease that is histologically characterized by diffuse mononuclear cell infiltrates and loosely formed granulomas in the lungs. We have previously reported that interleukin-17A (IL-17A) contributes to the development of experimental HP, and that the pattern recognition receptor Toll-like receptor 6 (TLR6) might be a factor in the initiation of this response. Using a well-established murine model of Saccharopolyspora rectivirgula-induced HP, we investigated the role of TLR6 in the immunopathogenesis of this disease. In the absence of TLR6 signalling, mice that received multiple challenges with S. rectivirgula-antigen (SR-Ag) had significantly less lung inflammation compared with C57BL/6 mice (wild-type; WT) similarly challenged with SR-Ag. Flow cytometric analysis of whole lung samples from SR-Ag-challenged mice showed that TLR6(-/-) mice had a decreased CD4(+) : CD8(+) T-cell ratio compared with WT mice. Cytokine analysis at various days after the final SR-Ag challenge revealed that whole lungs from TLR6(-/-) mice contained significantly less IL-17A than lungs from WT mice with HP. The IL-17A-driving cytokines IL-21 and IL-23 were also expressed at lower levels in SR-Ag-challenged TLR6(-/-) mice, when compared with SR-Ag-challenged WT mice. Other pro-inflammatory cytokines, namely interferon-gamma and RANTES, were also found to be regulated by TLR6 signalling. Anti-TLR6 neutralizing antibody treatment of dispersed lung cells significantly impaired SR-Ag-induced IL-17A and IL-6 generation. Together, these results indicate that TLR6 plays a pivotal role in the development and severity of HP via its role in IL-17A production.
Indexed as
Identifiers
What OpenQuestion holds
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.