1. TAMs play a crucial role in cancer progression, but the contributions and regulation of different macrophage subpopulations remain unclear.
2. Treatment with clodronate liposomes reduced proliferating macrophages in pancreatic cancer models, which increased CD8+ T cell infiltration and promoted CD8+ T cell spatial redistribution in tumors.
3. Targeting proliferating tumor-infiltrating macrophages may contribute to the antitumor effect.
The article is generally reliable and trustworthy, as it provides evidence from both human and mouse pancreatic ductal adenocarcinoma (PDAC) models to support its claims. The article also cites relevant studies to back up its assertions, such as Lavine et al.'s study on the contribution of embryo-derived TRMs and monocyte-derived TAMs to tumor growth in a pancreatic cancer mouse model [9]. Furthermore, the article does not appear to be biased or one-sided, as it presents both sides of the argument equally. It also does not contain any promotional content or partiality towards any particular point of view.
However, there are some points that could be improved upon in terms of trustworthiness and reliability. For example, the article does not provide any evidence for its claim that targeting proliferating tumor-infiltrating macrophages may increase CD8+ cytotoxic lymphocyte (CTL) infiltration and facilitate the spatial redistribution of CD8+ T cells in tumors, contributing to the antitumor effect. Additionally, possible risks associated with targeting proliferating tumor-infiltrating macrophages are not noted in the article. Finally, while the article mentions potential benefits of targeting TAMs for cancer treatment, it does not explore any potential counterarguments or drawbacks associated with this approach.