New insights into the role of VIP on the ratio of T-cell subsets during the development of autoimmune diabetes
Published 2010 View Full Article
- Home
- Publications
- Publication Search
- Publication Details
Title
New insights into the role of VIP on the ratio of T-cell subsets during the development of autoimmune diabetes
Authors
Keywords
-
Journal
IMMUNOLOGY AND CELL BIOLOGY
Volume 88, Issue 7, Pages 734-745
Publisher
Wiley
Online
2010-03-23
DOI
10.1038/icb.2010.29
References
Ask authors/readers for more resources
Related references
Note: Only part of the references are listed.- Vasoactive Intestinal Peptide as a Healing Mediator in Crohn’s Disease
- (2017) A. Arranz et al. NEUROIMMUNOMODULATION
- Cutting Edge: Vasoactive Intestinal Peptide (VIP) Induces Differentiation of Th17 Cells with a Distinctive Cytokine Profile
- (2014) M. Yadav et al. JOURNAL OF IMMUNOLOGY
- Development of Proteoglycan-Induced Arthritis Is Independent of IL-17
- (2014) P. D. Doodes et al. JOURNAL OF IMMUNOLOGY
- Regulation of the foxp3 Gene by the Th1 Cytokines: The Role of IL-27-Induced STAT1
- (2014) N. Ouaked et al. JOURNAL OF IMMUNOLOGY
- Role of Pituitary Adenylate Cyclase-Activating Polypeptide in the Pancreatic Endocrine System
- (2009) Bo Ahrén Annals of the New York Academy of Sciences
- Vasoactive Intestinal Peptide-Mediated Th17 Differentiation
- (2009) Mahesh Yadav et al. Annals of the New York Academy of Sciences
- IL-17 and Th17 Cells
- (2009) Thomas Korn et al. Annual Review of Immunology
- Th17 cells promote pancreatic inflammation but only induce diabetes efficiently in lymphopenic hosts after conversion into Th1 cells
- (2009) Natalia Martin-Orozco et al. EUROPEAN JOURNAL OF IMMUNOLOGY
- Highly purified Th17 cells from BDC2.5NOD mice convert into Th1-like cells in NOD/SCID recipient mice
- (2009) David Bending et al. JOURNAL OF CLINICAL INVESTIGATION
- The role of inflammation in insulitis and β-cell loss in type 1 diabetes
- (2009) Décio L. Eizirik et al. Nature Reviews Endocrinology
- Vasoactive intestinal peptide inhibits TNF-α-induced apoptotic events in acinar cells from nonobese diabetic mice submandibular glands
- (2009) Mario Calafat et al. ARTHRITIS RESEARCH & THERAPY
- CD4 T cells: fates, functions, and faults
- (2008) J. Zhu et al. BLOOD
- Cytokine-induced β-cell apoptosis is NO-dependent, mitochondria-mediated and inhibited by BCL-XL
- (2008) C. Holohan et al. JOURNAL OF CELLULAR AND MOLECULAR MEDICINE
- T Regulatory Cells in Autoimmune Diabetes: Past Challenges, Future Prospects
- (2008) Jeffrey A. Bluestone et al. JOURNAL OF CLINICAL IMMUNOLOGY
- Molecular Mechanisms of Regulatory T Cell Development
- (2008) Talal Chatila JOURNAL OF CLINICAL IMMUNOLOGY
- Interplay Between Effector Th17 and Regulatory T Cells
- (2008) Amit Awasthi et al. JOURNAL OF CLINICAL IMMUNOLOGY
- VIP reverses the expression profiling of TLR4-stimulated signaling pathway in rheumatoid arthritis synovial fibroblasts
- (2008) Alicia Arranz et al. MOLECULAR IMMUNOLOGY
- Vasoactive intestinal peptide suppresses toll-like receptor 4 expression in macrophages via Akt1 reducing their responsiveness to lipopolysaccharide
- (2008) Alicia Arranz et al. MOLECULAR IMMUNOLOGY
- The defect in T-cell regulation in NOD mice is an effect on the T-cell effectors
- (2008) A. M. D'Alise et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- IL-21 signaling is critical for the development of type I diabetes in the NOD mouse
- (2008) R. Spolski et al. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
- Immunoregulatory properties of vasoactive intestinal peptide in human T cell subsets: Implications for rheumatoid arthritis
- (2007) Irene Gutiérrez-Cañas et al. BRAIN BEHAVIOR AND IMMUNITY
Find Funding. Review Successful Grants.
Explore over 25,000 new funding opportunities and over 6,000,000 successful grants.
ExplorePublish 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 More