Journal
IMMUNOLOGY
Volume 135, Issue 2, Pages 112-124Publisher
WILEY-BLACKWELL
DOI: 10.1111/j.1365-2567.2011.03522.x
Keywords
autoimmune inflammation; briakinumab; inflammatory bowel disease; interleukin-23; psoriasis; rheumatoid arthritis; ustekinumab
Categories
Funding
- Important National Science & Technology Specific Projects of China [2009ZX09103-033]
- National Natural Science Foundation of China [30772647]
- Fundamental Research Funds for the Central Universities of China [2J10023]
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available