colleagues demonstrated that levels of TH2 inflammatory cytokines, such as interleukin (IL)-13, and levels of TSLP-activated dendritic cells were higher in breast tumors than in surrounding tissues. In their study, however, the source of TSLP was the cancer cells, rather than tumor-infiltrating fibroblasts. Accordingly, the investigators detected TSLP in supernatants from five different breast cancer cell lines and in 35 of 38 primary breast tumor samples. Administration of antibodies directed against TSLP or against TSLP-activated dendritic cells reduced tumor development in a xenograft mouse model.

The two studies suggest that blockade of TSLP might be a new strategy for the treatment of patients with breast or pancreatic cancer. As TSLP is known for its role in inflammation, efforts to block TSLP pharmaceutically are already underway, which could speed up the translation of these findings into clinical practice. For Palucka and her team, the next steps are to unravel “the mechanisms allowing TSLP release from cancer cells and...[to study] the impact of IL-13 on cancer cells.”