AI Article Synopsis
- The tumor microenvironment is complex and myeloid cells, like macrophages and neutrophils, are crucial in cancer growth from start to spread.
- Myeloid cells can adapt to different signals, displaying various activation states, with M1 and M2 macrophages exemplifying this flexibility.
- New research shows neutrophils can also interact with other cells and produce various cytokines, highlighting their role alongside macrophages in regulating immune responses in cancer and inflammation.
Article Abstract
The tumor microenvironment is a complex framework, in which myeloid cells play important roles in sculpting cancer development from tumor initiation to metastasis. Immune cells are key participants of the tumor microenvironment where they can promote or inhibit cancer formation and development. Plasticity is a widely accepted hallmark of myeloid cells and in particular of the monocyte-macrophage lineage. It includes the ability to display a wide spectrum of activation states in response to distinct signals and classical M1 or alternative M2 macrophages represent a paradigm of this feature. Neutrophils have long been viewed as terminally differentiated effector cells, playing a major role during the acute phase of inflammation and resistance against microbes. Recent evidence questioned this limited point of view, indicating that neutrophils can interact with distinct cell populations and produce a wide number of cytokines and effector molecules. Therefore, macrophages and neutrophils are both integrated in the regulation of the innate and adaptive immune responses in various inflammatory situations, including cancer.
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| http://dx.doi.org/10.1016/j.imbio.2013.06.003 | DOI Listing |
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