IL-25 is a cytokine that shares the sequence similarity with IL-17. This cytokine can induce NF-κB activation, and stimulate the production of IL-8. Both this cytokine and IL17B are ligands for the cytokine receptor IL17RB. Studies of the similar gene in mice suggested that this cytokine may be a proinflammatory cytokine favoring Th2-type immune response. Two alternatively spliced transcript variants of this gene encoding distinct isoforms have been reported.[4]
IL-25 induces the production of other cytokines, including IL-4, IL-5 and IL-13 in multiple tissues, which stimulate the expansion of eosinophils. This cytokine is an important molecule controlling immunity of the gut[7] and has been implicated in chronic inflammation associated with the gastrointestinal tract. IL-25 can kill some types of breast cancer cells.[8]
Further, the IL-25 gene has been identified in a chromosomal region associated with (autoimmune deleted, IBD not defined as autoimmune) diseases of the gut such as inflammatory bowel disease (IBD), although no direct evidence suggests that IL-25 plays any role in this disease.[9]
IL-25 has potent antitumor activity in vivo in several human cancers including melanoma, breast, lung, colon, and pancreatic cancers, suggesting the potential clinical use of IL-17E as an anticancer agent.[10]
↑Büning C, Genschel J, Weltrich R, Lochs H, Schmidt H (Oct 2003). "The interleukin-25 gene located in the inflammatory bowel disease (IBD) 4 region: no association with inflammatory bowel disease". European Journal of Immunogenetics. 30 (5): 329–33. doi:10.1046/j.1365-2370.2003.00411.x. PMID14641539.
↑Benatar T, Cao MY, Lee Y, Lightfoot J, Feng N, Gu X, Lee V, Jin H, Wang M, Wright JA, Young AH (Jun 2010). "IL-17E, a proinflammatory cytokine, has antitumor efficacy against several tumor types in vivo". Cancer Immunology, Immunotherapy. 59 (6): 805–17. doi:10.1007/s00262-009-0802-8. PMID20012860.
Pan G, French D, Mao W, Maruoka M, Risser P, Lee J, Foster J, Aggarwal S, Nicholes K, Guillet S, Schow P, Gurney AL (Dec 2001). "Forced expression of murine IL-17E induces growth retardation, jaundice, a Th2-biased response, and multiorgan inflammation in mice". Journal of Immunology. 167 (11): 6559–67. doi:10.4049/jimmunol.167.11.6559. PMID11714825.
Kim MR, Manoukian R, Yeh R, Silbiger SM, Danilenko DM, Scully S, Sun J, DeRose ML, Stolina M, Chang D, Van GY, Clarkin K, Nguyen HQ, Yu YB, Jing S, Senaldi G, Elliott G, Medlock ES (Oct 2002). "Transgenic overexpression of human IL-17E results in eosinophilia, B-lymphocyte hyperplasia, and altered antibody production". Blood. 100 (7): 2330–40. doi:10.1182/blood-2002-01-0012. PMID12239140.
Létuvé S, Lajoie-Kadoch S, Audusseau S, Rothenberg ME, Fiset PO, Ludwig MS, Hamid Q (Mar 2006). "IL-17E upregulates the expression of proinflammatory cytokines in lung fibroblasts". The Journal of Allergy and Clinical Immunology. 117 (3): 590–6. doi:10.1016/j.jaci.2005.10.025. PMID16522458.
Tamachi T, Maezawa Y, Ikeda K, Kagami S, Hatano M, Seto Y, Suto A, Suzuki K, Watanabe N, Saito Y, Tokuhisa T, Iwamoto I, Nakajima H (Sep 2006). "IL-25 enhances allergic airway inflammation by amplifying a TH2 cell-dependent pathway in mice". The Journal of Allergy and Clinical Immunology. 118 (3): 606–14. doi:10.1016/j.jaci.2006.04.051. PMID16950278.