The IL-23/Th17 Axis in the Immunopathogenesis of Psoriasis
Author:
Publisher
Elsevier BV
Subject
Cell Biology,Dermatology,Molecular Biology,Biochemistry
Reference152 articles.
1. Blockade of T lymphocyte costimulation with cytotoxic T lymphocyte-associated antigen 4-immunoglobulin (CTLA4Ig) reverses the cellular pathology of psoriatic plaques, including the activation of keratinocytes, dendritic cells, and endothelial cells;Abrams;J Exp Med,2000
2. Interleukins 1beta and 6 but not transforming growth factor-beta are essential for the differentiation of interleukin 17-producing human T helper cells;Acosta-Rodriguez;Nat Immunol,2007
3. Surface phenotype and antigenic specificity of human interleukin 17-producing T helper memory cells;Acosta-Rodriguez;Nat Immunol,2007
4. Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17;Aggarwal;J Biol Chem,2003
5. Interleukin-17 is produced by both Th1 and Th2 lymphocytes, and modulates interferon-gamma- and interleukin-4-induced activation of human keratinocytes;Albanesi;J Invest Dermatol,2000
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1. IL-23 induces CLEC5A+ IL-17A+ neutrophils and elicit skin inflammation associated with psoriatic arthritis;Journal of Autoimmunity;2024-02
2. A BET inhibitor, NHWD-870, can downregulate dendritic cells maturation via the IRF7-mediated signaling pathway to ameliorate imiquimod-induced psoriasis-like murine skin inflammation;European Journal of Pharmacology;2024-02
3. High-dimensional profiling of regulatory T cells in psoriasis reveals an impaired skin-trafficking property;eBioMedicine;2024-02
4. Etiopathogenesis of Psoriasis: Integration of Proposed Theories;Immunological Investigations;2024-01-19
5. Bibliometric analysis and description of research trends on T cells in psoriasis over the past two decades (2003–2022);Heliyon;2024-01
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