The sialic shield of leukemia cells.

Immune cells continually detect, engulf, and destroy invasive microbes and cancer cells. This process, called phagocytosis, is carried out by macrophages that must distinguish between proengulfment signals and inhibitory ("don't-eat-me") warnings (1). Cluster of differentiation 47 (CD47), a cell-surface receptor, is the archetypal don't-eat-me signal. Many cancers upregulate CD47 expression to escape phagocytosis, and CD47 blockade promotes phagocytosis of cancer cells in mice (2). However, CD47 blockers have not shown clinical benefits in patients with acute myeloid leukemia (AML), an aggressive cancer of blood immune cells (3–5). This discrepancy has raised the possibility that the molecular programs that inhibit phagocytosis differ between mice and humans (6). On page 174 of this issue, Chung et al. (7) report that the mechanisms that control macrophage function in human and mouse cells are indeed different. They also identify cluster of differentiation 43 (CD43) as a potential target for human AML treatment. [ABSTRACT FROM AUTHOR]