Chemotherapy has been a standard treatment for cancer for the past several decades and has long been suspected to cause systemic immune suppression. However, in recent years it has become clear that the immune status of a patient is an independent prognostic factor for chemotherapeutic efficacy, and that T-cell-mediated responses actively contribute to the tumor destruction triggered by some chemotherapeutic agents. In this respect, the induction of immunogenic cell death by these compounds appears to be crucial. In this issue of the European Journal of Immunology, a study by Hannesdóttir et al. [Eur. J. Immunol. 2013. 43: 2718-2729] demonstrates a crucial role for the IFN signaling molecule STAT1 during doxorubicin and Lapatinib treatment of HER2/Neu-driven mammary carcinomas. The genotoxic anthracycline doxorubicin causes immunogenic cancer cell death and is expected to depend on the immune system, but the dual ErbB2/HER2/Neu and ErbB1/EGFR inhibitor Lapatinib also turns out to cause immune reactivity. Although CD8+ T cells are partially involved in this phenomenon, doxorubicin, and Lapatinib also affect the myeloid infiltrate (i.e. tumor-associated macrophages and monocytes) in tumors. In this Commentary, we place these findings in the context of current knowledge and propose new avenues for future research.
|Number of pages||5|
|Journal||European Journal of Immunology|
|Publication status||Published - 10 Oct 2013|
- Antitumor immunity CD8 + T cells Doxorubicin
- Lapatinib Stat1