期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 208, 期 3, 页码 479-490出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20102131
关键词
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资金
- Baylor Health Care Systems Foundation
- National Institutes of Health [R0-1 CA89440, R21 41056001, U19 Al057234, R0-1 CA78846, CA85540]
The human breast tumor microenvironment can display features of T helper type 2 (Th2) inflammation, and Th2 inflammation can promote tumor development. However, the molecular and cellular mechanisms contributing to Th2 inflammation in breast tumors remain unclear. Here, we show that human breast cancer cells produce thymic stromal lymphopoietin (TSLP). Breast tumor supernatants, in a TSLP-dependent manner, induce expression of OX4OL on dendritic cells (DCs). OX40L(+) DCs are found in primary breast tumor infiltrates. OX40L(+) DCs drive development of inflammatory Th2 cells producing interleukin-13 and tumor necrosis factor in vitro. Antibodies neutralizing TSLP or OX4OL inhibit breast tumor growth and interleukin-13 production in a xenograft model. Thus, breast cancer cell-derived TSLP contributes to the inflammatory Th2 microenvironment conducive to breast tumor development by inducing OX4OL expression on DCs.
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