A cytokine-mediated link between innate immunity, inflammation, and cancer
Journal
Journal of Clinical Investigation
Journal Volume
117
Journal Issue
5
Pages
1175-1183
Date Issued
2007
Author(s)
Karin M.
Abstract
It has been established that cancer can be promoted and/or exacerbated by inflammation and infections. Indeed, chronic inflammation orchestrates a tumor-supporting microenvironment that is an indispensable participant in the neoplastic process. The mechanisms that link infection, innate immunity, inflammation, and cancer are being unraveled at a fast pace. Important components in this linkage are the cytokines produced by activated innate immune cells that stimulate tumor growth and progression. In addition, soluble mediators produced by cancer cells recruit and activate inflammatory cells, which further stimulate tumor progression. However, inflammatory cells also produce cytokines that can limit tumor growth. Here we provide an overview of the current understanding of the role of inflammation-induced cytokines in tumor initiation, promotion, and progression.
SDGs
Other Subjects
cytokine; I kappa B; interleukin 10; interleukin 12; interleukin 17; interleukin 23; interleukin 6; transforming growth factor beta; tumor necrosis factor alpha; tumor necrosis factor alpha antibody; tumor necrosis factor related apoptosis inducing ligand; antineoplastic activity; apoptosis; cancer; carcinogenesis; cell infiltration; cell survival; chronic inflammation; cytokine production; disease association; gene mutation; genetic polymorphism; human; immunocompetent cell; infection; inflammatory cell; innate immunity; nonhuman; priority journal; protein binding; protein expression; protein phosphorylation; review; signal transduction; tumor associated leukocyte; tumor growth; upregulation; Animals; Cytokines; Humans; Immunity, Natural; Inflammation; Neoplasms
Type
review