Dendritic cells provide a potential link between smoking and inflammation in rheumatoid arthritis
Published 2012 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
Dendritic cells provide a potential link between smoking and inflammation in rheumatoid arthritis
Authors
Keywords
-
Journal
ARTHRITIS RESEARCH & THERAPY
Volume 14, Issue 5, Pages R208
Publisher
Springer Nature
Online
2012-10-04
DOI
10.1186/ar4046
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Interleukin-17A upregulates receptor activator of NF-κB on osteoclast precursors
- (2012) Iannis E Adamopoulos et al. ARTHRITIS RESEARCH & THERAPY
- Fate mapping of IL-17-producing T cells in inflammatory responses
- (2011) Keiji Hirota et al. NATURE IMMUNOLOGY
- Prevention of autoimmune rheumatic disease: state of the art and future perspectives
- (2010) L. Klareskog et al. ANNALS OF THE RHEUMATIC DISEASES
- Genetic variants in the prediction of rheumatoid arthritis
- (2010) A. H. M. van der Helm-van Mil et al. ANNALS OF THE RHEUMATIC DISEASES
- Patients with early rheumatoid arthritis who smoke are less likely to respond to treatment with methotrexate and tumor necrosis factor inhibitors: Observations from the Epidemiological Investigation of Rheumatoid Arthritis and the Swedish Rheumatology Reg
- (2010) Saedis Saevarsdottir et al. ARTHRITIS AND RHEUMATISM
- An Interaction between Kynurenine and the Aryl Hydrocarbon Receptor Can Generate Regulatory T Cells
- (2010) J. D. Mezrich et al. JOURNAL OF IMMUNOLOGY
- Rheumatoid arthritis
- (2010) David L Scott et al. LANCET
- Aryl hydrocarbon receptor negatively regulates dendritic cell immunogenicity via a kynurenine-dependent mechanism
- (2010) N. T. Nguyen et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Functional and phenotypic effects of AhR activation in inflammatory dendritic cells
- (2010) Jaishree Bankoti et al. TOXICOLOGY AND APPLIED PHARMACOLOGY
- Prevalence of and predictive factors for sustained disease-modifying antirheumatic drug-free remission in rheumatoid arthritis: Results from two large early arthritis cohorts
- (2009) Diane van der Woude et al. ARTHRITIS AND RHEUMATISM
- Autoimmunity to specific citrullinated proteins gives the first clues to the etiology of rheumatoid arthritis
- (2009) Natalia Wegner et al. IMMUNOLOGICAL REVIEWS
- Anti-TNF-α Agents Are Less Effective for the Treatment of Rheumatoid Arthritis in Current Smokers
- (2009) A Abhishek et al. JCR-JOURNAL OF CLINICAL RHEUMATOLOGY
- Monocyte Derived Interleukin (IL)-23 Is an Important Determinant of Synovial IL-17A Expression in Rheumatoid Arthritis
- (2009) L. K. STAMP et al. JOURNAL OF RHEUMATOLOGY
- Specific interaction between genotype, smoking and autoimmunity to citrullinated α-enolase in the etiology of rheumatoid arthritis
- (2009) Hiba Mahdi et al. NATURE GENETICS
- Human rheumatoid arthritis tissue production of IL-17A drives matrix and cartilage degradation: synergy with tumour necrosis factor-α, Oncostatin M and response to biologic therapies
- (2009) Ellen M Moran et al. ARTHRITIS RESEARCH & THERAPY
- Smoking increases peptidylarginine deiminase 2 enzyme expression in human lungs and increases citrullination in BAL cells
- (2008) D Makrygiannakis et al. ANNALS OF THE RHEUMATIC DISEASES
- The aryl hydrocarbon receptor links TH17-cell-mediated autoimmunity to environmental toxins
- (2008) Marc Veldhoen et al. NATURE
- The Search for Endogenous Activators of the Aryl Hydrocarbon Receptor
- (2007) Linh P. Nguyen et al. CHEMICAL RESEARCH IN TOXICOLOGY
- IL-17/Th17 targeting: On the road to prevent chronic destructive arthritis?
- (2007) Erik Lubberts CYTOKINE
Publish scientific posters with Peeref
Peeref publishes scientific posters from all research disciplines. Our Diamond Open Access policy means free access to content and no publication fees for authors.
Learn MoreCreate your own webinar
Interested in hosting your own webinar? Check the schedule and propose your idea to the Peeref Content Team.
Create Now