Therapeutics targeting CD47 represent a new strategy for treating cancer. The CD47/SIRPα axis, a myeloid-specific immune checkpoint, limits macrophage removal of HSCs but can be exploited by hematologic and solid malignancies. Furthermore, insights into myeloid development have informed us of mechanisms of programmed cell removal. Defects in myelopoiesis contribute to many hematologic disorders, and some of these can be overcome with therapies that target the aberrant stage of development.
Hematopoiesis also changes over time, with a bias of the dominating HSCs towards myeloid development as animals age. Some adult myeloid populations develop directly from yolk sac progenitors without apparent bone marrow intermediates, such as tissue resident macrophages. The stages of hematopoiesis have been defined in both mice and humans.ĭuring embryological development, the earliest hematopoiesis takes place in yolk sac blood islands then migrates to the fetal liver and hematopoietic organs. The myeloid arm is characterized by the Common Myeloid Progenitor and all of its resulting cell types. The hematopoietic lineage is divided into two main branches: the myeloid and lymphoid arms. Since its first purification in 1988, additional studies have refined the phenotype and functionality of HSCs and characterized all of their downstream progeny. The hematopoietic stem cell (HSC) is a multipotent stem cell that resides in the bone marrow and has the ability to form all of the cells of the blood and immune system.
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