IL-17-producing γδ T cells and neutrophils conspire to promote breast cancer metastasis.

ABSTRACT: Metastatic disease remains the primary cause of death for patients with breast cancer. The different steps of the metastatic cascade rely on reciprocal interactions between cancer cells and their microenvironment. Within this local microenvironment and in distant organs, immune cells and their mediators are known to facilitate metastasis formation. However, the precise contribution of tumour-induced systemic inflammation to metastasis and the mechanisms regulating systemic inflammation are poorly understood. Here we show that tumours maximize their chance of metastasizing by evoking a systemic inflammatory cascade in mouse models of spontaneous breast cancer metastasis. We mechanistically demonstrate that interleukin (IL)-1β elicits IL-17 expression from gamma delta (γδ) T cells, resulting

SUBMITTER: Coffelt SB 

PROVIDER: S-EPMC4475637 | biostudies-literature | 2015 Jun

REPOSITORIES: biostudies-literature