Suppression of Immune Induction of Collagen-Induced Arthritis in IL-17-Deficient Mice 1
By S. Nakae, Aya Nambu, K. Sudo, Y. Iwakura. Journal of Immunology, 2003
1,424 citations recorded by the source corpus.
Subfields: Oncology, Radiology, Nuclear Medicine and Imaging, Rheumatology
View Paper: https://www.semanticscholar.org/paper/dc29a2f6aa07a43830e9bbb05f9f236c3ac28746
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Citations in the corpus
- The IL-23/Th17 axis in the immunopathogenesis of psoriasis. (2009, background): “IL-17-deficient mice are resistant to adjuvant-induced arthritis (Nakae et al., 2003) and develop EAE with delayed onset and reduced severity (Komiyama et al.”
- Th17 cells promote cytotoxic T cell activation in tumor immunity (2009, background): “, 2001) and resistance to autoimmune diseases (Langrish et al., 2005; Nakae et al., 2003; Park et al., 2005; Yang et al., 2008).”
- IL-17 family cytokines and the expanding diversity of effector T cell lineages. (2007, background): “Consistent with this, mice with a targeted deletion of the Il17a gene alone have a profound phenotype that does not appear to be compensated by intact Il17f expression (65, 66).”
- Interleukin (IL)-22 and IL-17 are coexpressed by Th17 cells and cooperatively enhance expression of antimicrobial peptides (2006, background): “For example, IL-23p19–defi cient mice are completely resistant to disease in collagen-induced arthritis, whereas IL-17A– defi cient mice remain susceptible, albeit with a signifi cantly reduced incidence and severity (9, 10).”
- Dectin-2 recognition of alpha-mannans and induction of Th17 cell differentiation is essential for host defense against Candida albicans. (2010, background): “We and others have shown that IL-17A plays important roles not only in the development of autoimmune diseases, but also in the host defense against bacteria (Mangan et al., 2006; Nakae et al., 2003; Schulz et al., 2008; Shiomi et al., 2008; Umemura et al., 2007; Ye et al., 2001).”