The parasitic helminth product ES-62 suppresses pathogenesis in collagen-induced arthritis by targeting the interleukin-17-producing cellular network at multiple sites
出版年份 2012 全文链接
标题
The parasitic helminth product ES-62 suppresses pathogenesis in collagen-induced arthritis by targeting the interleukin-17-producing cellular network at multiple sites
作者
关键词
-
出版物
ARTHRITIS AND RHEUMATISM
Volume 64, Issue 10, Pages 3168-3178
出版商
Wiley
发表日期
2012-06-22
DOI
10.1002/art.34581
参考文献
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- (2014) C. Collins et al. JOURNAL OF IMMUNOLOGY
- Immunomodulatory Properties of ES-62, a Phosphorylcholine - Containing Glycoprotein Secreted by Acanthocheilonema viteae
- (2012) Lamyaa Al-Riyami et al. Endocrine Metabolic & Immune Disorders-Drug Targets
- Local expression of interleukin-27 ameliorates collagen-induced arthritis
- (2011) Sarah R. Pickens et al. ARTHRITIS AND RHEUMATISM
- Th17 Cells Induce Colitis and Promote Th1 Cell Responses through IL-17 Induction of Innate IL-12 and IL-23 Production
- (2011) T. Feng et al. JOURNAL OF IMMUNOLOGY
- Insights into the role of Toll-like receptors in modulation of T cell responses
- (2010) Raveendra Kulkarni et al. CELL AND TISSUE RESEARCH
- Complement C5a regulates IL-17 by affecting the crosstalk between DC and γδ T cells in CLP-induced sepsis
- (2010) Ruonan Xu et al. EUROPEAN JOURNAL OF IMMUNOLOGY
- γδd T cells promote the maturation of dendritic cells during West Nile virus infection
- (2010) Hao Fang et al. FEMS IMMUNOLOGY AND MEDICAL MICROBIOLOGY
- γδ T Cells Enhance Autoimmunity by Restraining Regulatory T Cell Responses via an Interleukin-23-Dependent Mechanism
- (2010) Franziska Petermann et al. IMMUNITY
- Toll-like Receptor 2 Signaling in CD4+ T Lymphocytes Promotes T Helper 17 Responses and Regulates the Pathogenesis of Autoimmune Disease
- (2010) Joseph M. Reynolds et al. IMMUNITY
- The Receptor SIGIRR Suppresses Th17 Cell Proliferation via Inhibition of the Interleukin-1 Receptor Pathway and mTOR Kinase Activation
- (2010) Muhammet F. Gulen et al. IMMUNITY
- IL-17A-Producing T Cells Promote CTL Responses against Listeria monocytogenes Infection by Enhancing Dendritic Cell Cross-Presentation
- (2010) S. Xu et al. JOURNAL OF IMMUNOLOGY
- Gamma/delta T cells are the predominant source of interleukin-17 in affected joints in collagen-induced arthritis, but not in rheumatoid arthritis
- (2009) Yoshinaga Ito et al. ARTHRITIS AND RHEUMATISM
- Interleukin-17-Producing γδ T Cells Selectively Expand in Response to Pathogen Products and Environmental Signals
- (2009) Bruno Martin et al. IMMUNITY
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- (2009) Caroline E. Sutton et al. IMMUNITY
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- (2009) K. A. Staschke et al. JOURNAL OF IMMUNOLOGY
- IL-27 Is a Key Regulator of IL-10 and IL-17 Production by Human CD4+ T Cells
- (2009) G. Murugaiyan et al. JOURNAL OF IMMUNOLOGY
- Effector mechanisms of interleukin-17 in collagen-induced arthritis in the absence of interferon-γ and counteraction by interferon-γ
- (2009) Hilde Kelchtermans et al. ARTHRITIS RESEARCH & THERAPY
- Interleukin 27 attenuates collagen-induced arthritis
- (2008) W Niedbala et al. ANNALS OF THE RHEUMATIC DISEASES
- Signalling adaptors used by Toll-like receptors: An update
- (2008) Elaine F. Kenny et al. CYTOKINE
- Enhanced secretion of interferon-γ by bovine γδ T cells induced by coculture withMycobacterium bovis-infected dendritic cells: evidence for reciprocal activating signals
- (2008) Sally J. Price et al. IMMUNOLOGY
- TH-17 cells in rheumatoid arthritis
- (2008) Shiva Shahrara et al. ARTHRITIS RESEARCH & THERAPY
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