Inhibiting Stat3 signaling in the hematopoietic system elicits multicomponent antitumor immunity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2005-12

AUTHORS

Marcin Kortylewski, Maciej Kujawski, Tianhong Wang, Sheng Wei, Shumin Zhang, Shari Pilon-Thomas, Guilian Niu, Heidi Kay, James Mulé, William G Kerr, Richard Jove, Drew Pardoll, Hua Yu

ABSTRACT

The immune system can act as an extrinsic suppressor of tumors. Therefore, tumor progression depends in part on mechanisms that downmodulate intrinsic immune surveillance. Identifying these inhibitory pathways may provide promising targets to enhance antitumor immunity. Here, we show that Stat3 is constitutively activated in diverse tumor-infiltrating immune cells, and ablating Stat3 in hematopoietic cells triggers an intrinsic immune-surveillance system that inhibits tumor growth and metastasis. We observed a markedly enhanced function of dendritic cells, T cells, natural killer (NK) cells and neutrophils in tumor-bearing mice with Stat3(-/-) hematopoietic cells, and showed that tumor regression requires immune cells. Targeting Stat3 with a small-molecule drug induces T cell- and NK cell-dependent growth inhibition of established tumors otherwise resistant to direct killing by the inhibitor. Our findings show that Stat3 signaling restrains natural tumor immune surveillance and that inhibiting hematopoietic Stat3 in tumor-bearing hosts elicits multicomponent therapeutic antitumor immunity. More... »

PAGES

1314-1321

Journal

TITLE

Nature Medicine

ISSUE

12

VOLUME

11

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm1325

DOI

http://dx.doi.org/10.1038/nm1325

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1009280775

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/16288283


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