TAMable tumor-associated macrophages in response to innate RNA sensing

Abstract

Antitumor effect of PolyI:C (a viral dsRNA analog) has been attributed to dendritic cell (DC)-maturation activity, that drives antitumor NK cells, DC cross-presentation, cytotoxic T lymphocytes and many IFN-inducible genes. According to a recent paper, tumor-infiltrating M2 macrophages are found to become an additional antitumor effector through polyI:C response.

Figure 1. PolyI:C induces three antitumor effectors via different routes. Antitumor activity of polyI:C against tumor cells are assessed in mouse tumor-implant models. A unique point in this review is the third pathway where tumor-infiltrating myeloid cells are involved, effectively damages Lewis Lung carcinoma cells. This tumoricidal activity is mediated by the TICAM-1 pathway in the myeloid cells, and attributed to TNF-α. Although polyI:C is i.p. administered, it acts on tumor-infiltrating Mf and converts them to antitumor effectors.