Fig. 3
From: TAM receptors, Phosphatidylserine, inflammation, and Cancer
Inhibition of PtdSer-TAM signaling in tumor-immune interactions leads to elevated inflammation but may differentially affect tumor growth. Bone-marrow derived macrophages (BMDMs) differentially influence tumor progression in different cancer models. (a) Inhibition of MERTK in CD11b + BMDMs resulted in elevated inflammation, which conveyed anti-tumor immunity resulting in inhibited growth of breast, melanoma and MC38 colon cancer tumors [69]. (b) By contrast to (a), in a DSS-induced model of colon cancer, the dual inhibition of AXL and MERTK in BMDMs had no effect on tumor progression [76]. Instead, AXL and MERK inhibition in F4/80+; CD11b + lamina propria macrophages conveyed pro-tumor immunity, which promoted cancer progression. These data demonstrate that while inhibition of TAM signaling in macrophages led to inflammation in both cases, opposing effects were imparted on tumor growth, highlighting the complex liaisons between immune and tumor cells through inflammation. Such complexity is likely to be mediated by additional factors, some of which function by immune-modulation, others are yet to be revealed (depicted in the oval). See discussion in the main text