2011/10/17 by Chunlei Tang, Shu Chen, Hai Qian +1
Immunology and Microbiology · Medicine · #Dermatology and Skin Diseases #Immunodeficiency and Autoimmune Disorders #Psoriasis: Treatment and Pathogenesis
paper · pdf · doi:10.1111/j.1365-2567.2011.03522.x
openalex publication_date 2011/10/17 · crossref created 2011/10/17 · crossref issued 2012/01/11 · crossref published 2012/01/11 · crossref published-online 2012/01/11 · crossref published-print 2012/02/01 · crossref deposited 2023/09/04 · openalex created_date 2025/10/10 · crossref indexed 2026/07/29 · openalex updated_date 2026/07/30
Interleukin-23 (IL-23) is a member of the IL-12 family of cytokines with pro-inflammatory properties. Its ability to potently enhance the expansion of T helper type 17 (Th17) cells indicates the responsibility for many of the inflammatory autoimmune responses. Emerging data demonstrate that IL-23 is a key participant in central regulation of the cellular mechanisms involved in inflammation. Both IL-23 and IL-17 form a new axis through Th17 cells, which has evolved in response to human diseases associated with immunoactivation and immunopathogeny, including bacterial or viral infections and chronic inflammation. Targeting of IL-23 or the IL-23 receptor or IL-23 axis is a potential therapeutic approach for autoimmune diseases including psoriasis, inflammatory bowel disease, rheumatoid arthritis and multiple sclerosis. The current review focuses on the immunobiology of IL-23 and summarizes the most recent findings on the role of IL-23 in the pre-clinical and ongoing clinical studies.