IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway Export

@article{citeulike:5094120, abstract = {Although the Th17 subset and its signature cytokine, interleukin (IL)-17A (IL-17), are implicated in certain autoimmune diseases, their role in cancer remains to be further explored. IL-17 has been shown to be elevated in several types of cancer, but how it might contribute to tumor growth is still unclear. We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL-17-/- mice but drastically accelerated in IFN-{gamma}-/- mice, contributed to by elevated intratumoral IL-17, indicating a role of IL-17 in promoting tumor growth. Adoptive transfer studies and analysis of the tumor microenvironment suggest that CD4+ T cells are the predominant source of IL-17. Enhancement of tumor growth by IL-17 involves direct effects on tumor cells and tumor-associated stromal cells, which bear IL-17 receptors. IL-17 induces IL-6 production, which in turn activates oncogenic signal transducer and activator of transcription (Stat) 3, up-regulating prosurvival and proangiogenic genes. The Th17 response can thus promote tumor growth, in part via an IL-6-Stat3 pathway. 10.1084/jem.20090207}, author = {Wang, Lin and Yi, Tangsheng and Kortylewski, Marcin and Pardoll, Drew M. and Zeng, Defu and Yu, Hua}, citeulike-article-id = {5094120}, citeulike-linkout-0 = {http://dx.doi.org/10.1084/jem.20090207}, citeulike-linkout-1 = {http://jem.rupress.org/cgi/content/abstract/206/7/1457}, citeulike-linkout-2 = {http://view.ncbi.nlm.nih.gov/pubmed/19564351}, citeulike-linkout-3 = {http://www.hubmed.org/display.cgi?uids=19564351}, day = {6}, doi = {10.1084/jem.20090207}, journal = {J. Exp. Med.}, keywords = {il-17, th17, tumor-rejection}, month = {July}, number = {7}, pages = {1457--1464}, posted-at = {2009-07-08 20:36:22}, priority = {2}, title = {IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway}, url = {http://dx.doi.org/10.1084/jem.20090207}, volume = {206}, year = {2009} }

TY - JOUR ID - citeulike:5094120 L3 - citeulike-article-id:5094120 N2 - Although the Th17 subset and its signature cytokine, interleukin (IL)-17A (IL-17), are implicated in certain autoimmune diseases, their role in cancer remains to be further explored. IL-17 has been shown to be elevated in several types of cancer, but how it might contribute to tumor growth is still unclear. We show that growth of B16 melanoma and MB49 bladder carcinoma is reduced in IL-17-/- mice but drastically accelerated in IFN-{gamma}-/- mice, contributed to by elevated intratumoral IL-17, indicating a role of IL-17 in promoting tumor growth. Adoptive transfer studies and analysis of the tumor microenvironment suggest that CD4+ T cells are the predominant source of IL-17. Enhancement of tumor growth by IL-17 involves direct effects on tumor cells and tumor-associated stromal cells, which bear IL-17 receptors. IL-17 induces IL-6 production, which in turn activates oncogenic signal transducer and activator of transcription (Stat) 3, up-regulating prosurvival and proangiogenic genes. The Th17 response can thus promote tumor growth, in part via an IL-6-Stat3 pathway. 10.1084/jem.20090207 IS - 7 JF - J. Exp. Med. EP - 1464 TI - IL-17 can promote tumor growth through an IL-6-Stat3 signaling pathway VL - 206 SP - 1457 KW - il-17 KW - th17 KW - tumor-rejection AU - Wang, Lin AU - Yi, Tangsheng AU - Kortylewski, Marcin AU - Pardoll, Drew AU - Zeng, Defu AU - Yu, Hua PY - 2009/07/06/ UR - http://dx.doi.org/10.1084/jem.20090207 ER -