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Cell Press, Cancer Cell, 5(14), p. 408-419, 2008

DOI: 10.1016/j.ccr.2008.10.011

Cell Press, Cancer Cell, 6(14), p. 494, 2008

DOI: 10.1016/j.ccr.2008.11.004

Cell Press, Cancer Cell, 1(19), p. 154, 2011

DOI: 10.1016/j.ccr.2011.01.017

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Overexpression of Interleukin-1β Induces Gastric Inflammation and Cancer and Mobilizes Myeloid-Derived Suppressor Cells in Mice

Journal article published in 2008 by Shuiping Tu, Govind Bhagat ORCID, Guanglin Cui, Shigeo Takaishi, Evelyn A. Kurt-Jones, Barry Rickman, Kelly S. Betz, Melitta Penz-Oesterreicher, Olle Bjorkdahl, Olle Bjorkdhl, James G. Fox, Timothy C. Wang ORCID
This paper is available in a repository.
This paper is available in a repository.

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Abstract

Polymorphisms of interleukin-1beta (IL-1beta) are associated with an increased risk of solid malignancies. Here, we show that stomach-specific expression of human IL-1beta in transgenic mice leads to spontaneous gastric inflammation and cancer that correlate with early recruitment of myeloid-derived suppressor cells (MDSCs) to the stomach. IL-1beta activates MDSCs in vitro and in vivo through an IL-1RI/NF-kappaB pathway. IL-1beta transgenic mice deficient in T and B lymphocytes develop gastric dysplasia accompanied by a marked increase in MDSCs in the stomach. Antagonism of IL-1 receptor signaling inhibits the development of gastric preneoplasia and suppresses MDSC mobilization. These results demonstrate that pathologic elevation of a single proinflammatory cytokine may be sufficient to induce neoplasia and provide a direct link between IL-1beta, MDSCs, and carcinogenesis.