The research is about how TAMs (Tumor associated Macrophages) differ from MTMs (Mammary tissue macrophages) functionally and phenotypically. Not all macrophages help tumor growth but TAMs do. It was investigated that how TAM differentiate from its precursors and helps in tumor growth. RBPJ (transcriptional regulator of Notch signaling) helps TAMs. Investigation was done on myeloid cells during cancer progression. Myeloid cells consist of more than 50% of CD45+ cells and population I, II, III cells. Distinguishing Population I, II, III based on cell surface expression may not be accurate. So it was preferred to distinguish based on transcriptional phenotypes. Finally it was concluded that Population I cells are TAMs. i.e these cells helps tumor growth.
Ly6C+ CCR2+ inflammatory monocytes contribute to MTMs and lesser extent to TAMs. TAMs are derived from CCR2+ monocyte precursors but require less input from blood compared to MTMs. Higher proliferating capacity of TAMs is required to find their precursor. TAMs expressed higher levels of Ki67 staining and edU incorporation relative to MTMs. Monocytes could differentiate into TAMs invivo. TAMs differentiation pathway is distinct from MTMs pathway. TAMs are not AAMs (Alternatively Activated Macrophages). It was found that TAMs display a gene expression signature associated with Notch signaling pathway. TAMs depends on Notch signaling but TAM differentiation is not completely abolished in the absence of RBPJ (transcriptional regulator of Notch signaling). The data suggested a specific function of RBPJ dependent TAMs in promoting tumor immune tolerance in part by modulating the CD8+ cell response. It was hypothesized that control of adaptive immune response by TAMs is one among its role in tumor growth.
Reference: http://www.ncbi.nlm.nih.gov/pubmed/24812208
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