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- W4238698948 endingPage "635" @default.
- W4238698948 startingPage "615" @default.
- W4238698948 abstract "Microorganisms maintain an evolutionary advantage over their slowly replicating eukaryotic hosts. High mutation rates, rapid doubling times, and free genetic exchange between microbial species often place a considerable burden on the infected host to counter virulence escape mechanisms. This selective pressure has driven the acquisition of numerous eukaryotic defense strategies to protect host genome integrity and promote survival at the level of the individual cell (1). These cell-autonomous effector mechanisms, often considered unique to the immune cells of advanced metazoans, have in fact been largely inherited and repurposed from our eukaryotic ancestors (Fig. 1). For example, phagocytosis developed as a trophic mechanism in unicellular amoebae long before its adaptation as a tool for immunity in the specialized “immune-like” cells of early invertebrates (2,3). Amebocytes, hemocytes, and coelomocytes present in lower organisms likewise predate professional phagocytes in animals with their ability to bind, engulf, and kill foreign microorganisms (4)." @default.
- W4238698948 created "2022-05-12" @default.
- W4238698948 creator A5002945796 @default.
- W4238698948 creator A5015448925 @default.
- W4238698948 creator A5089455277 @default.
- W4238698948 date "2017-01-12" @default.
- W4238698948 modified "2023-10-06" @default.
- W4238698948 title "Evolution of Cell-Autonomous Effector Mechanisms in Macrophages versus Non-Immune Cells" @default.
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