Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis
By Yan Zheng, D. Danilenko, P. Valdez, I. Kasman, J. Eastham‐Anderson, Jianfeng Wu, Wenjun Ouyang. Nature, 2007
2,007 citations recorded by the source corpus.
Subfields: Dermatology, Immunology, Oncology
View Paper: https://www.semanticscholar.org/paper/528f245b7518968a986045017fb2a447cf7d9779
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Citations in the corpus
- CD8+ T cells and fatty acids orchestrate tumor ferroptosis and immunity via ACSL4 (2022, background): “…findings that the combination of different cytokines (such as TGF β plus IL-6) induces Th17 cells or Th22 cells (Cua et al., 2003; Mangan et al., 2006; Zheng et al., 2007), and the combination of TNF α and IFN γ induces PANoptosis as characterized by inflammatory cell death (Karki et al., 2021).”
- Anti- and Pro-inflammatory Roles of TGF-β, IL-10, and IL-22 In Immunity and Autoimmunity (2009, background): “In a mouse model of dermal inflammation in which IL-23 is directly applied to the ear, IL-22 was essential in mediating inflammation [60].”
- IL-17 is essential for host defense against cutaneous Staphylococcus aureus infection in mice. (2010, background): “β-defensins and cathelicidin) or by inducing epithelial proliferation, thereby increasing epithelial resistance to infection (28, 29, 41, 46, 47).”
- Th17 cells in human disease (2008, background): “Liang SC, et al. An IL-17F/A heterodimer protein is produced by mouse Th17 cells and induces airway neutrophil recruitment.”
- IL-22BP is regulated by the inflammasome and modulates tumorigenesis in the intestine (2012, neutral): “However, IL-22 can also promote pathological inflammatory responses in the skin 10 or intestine 11 in mouse models, and its concentration is increased in a variety of human diseases including psoriasis, rheumatoid arthritis, infections, and IBD 5 .”
- Psoriasis Pathogenesis and the Development of Novel, Targeted Immune Therapies (2017, neutral): “IL-17 also acts synergistically with TNF to potentiate IL-17–induced transcription of several proinflammatory genes (eg, TNF, IL-1b, IL-6, and IL-8),47-50 which activate mDCs and promote the differentiation of T17 cells in the skin and draining lymph nodes.32,51 Epidermal hyperplasia, a hallmark of ”