Antigen-specific T cell sensitization is impaired in IL-17-deficient mice, causing suppression of allergic cellular and humoral responses.

By S. Nakae, Yutaka Komiyama, Aya Nambu, K. Sudo, M. Iwase, I. Homma, K. Sekikawa, M. Asano, Y. Iwakura. Immunity, 2002

1,190 citations recorded by the source corpus.

Subfields: Immunology

View Paper: https://www.semanticscholar.org/paper/7d7769682e77b3f8db61b863ebc4e3b39f4dea40

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Citations in the corpus

• Interleukin-22 but not interleukin-17 provides protection to hepatocytes during acute liver inflammation. (2007, methodology): “IL-17A-deficient mice on a C57BL/6 stain (N9) were kindly provided by Y. Iwakura of the University of Tokyo, Japan (Nakae et al., 2002).”
• Interleukin 23 receptor is essential for terminal differentiation of effector T helper type 17 cells in vivo (2009, neutral): “To determine the functional ability of the Il23ra −/− OT-II T H 17 cells, we tested whether they could mediate an IL-17-dependent delayed-type hypersensitivity (DTH) reactio”
• A distinct lineage of CD4 T cells regulates tissue inflammation by producing interleukin 17 (2005, result): “IL-17 is also important in contact, delayed-type and airway hypersensitivities, as shown in a study using IL-17-deficient mic”
• IL-17-Mediated Regulation of Innate and Acquired Immune Response against Pulmonary Mycobacterium bovis Bacille Calmette-Guérin Infection1 (2007, methodology): “It has been reported that IL-17 is required to induce optimum Th1 and DTH responses against haptens (27), which is consistent with our observation that the Th1-type response is decreased in the absence of IL-17.”
• IL-23-Independent IL-17 Production Regulates Intestinal Epithelial Permeability (2015, neutral): “Il17 / , Rorc / , Rorc(gt)-GfpTG, Il23r-Gfp, and Tcrd / mice were derived as previously described and bred and housed within micro isolator caging units , at MRL (Awasthi et al., 2009; Ivanov et al., 2006; Lochner et al., 2008; Nakae et al., 2002).”