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Granulocyte colony-stimulating factor receptor (CSF3R) and Granulocyte-macrophage colony-stimulating factor receptor (CSF2R) are distinct members of the Type I cytokine receptor family that play essential roles in the production and activation of myeloid cells (UniProt: Q99062, P15509). CSF3R (also known as CD114) specifically binds G-CSF to drive the differentiation and proliferation of neutrophils; activating mutations in this receptor, most notably the T618I variant, are hallmark drivers of chronic neutrophilic leukemia (CNL) and atypical chronic myeloid leukemia (aCML) (PubMed: 23656643). CSF2R is a heteromeric complex (comprising alpha and beta subunits, CD116 and CD131) that binds GM-CSF, stimulating the production of both granulocytes and macrophages and acting as a key mediator in inflammatory diseases such as rheumatoid arthritis (PubMed: 28100480). Therapeutically, agonists like filgrastim and sargramostim are used to treat neutropenia and mobilize stem cells, while antagonists (e.g., mavrilimumab) and downstream signaling inhibitors (e.g., ruxolitinib) are utilized or investigated for treating inflammatory conditions and myeloid malignancies (NIH: StatPearls). This entry is marked as incorrect because it combines two distinct therapeutic targets into a single record.
Agonism of the receptor to stimulate myelopoiesis; antagonism of the receptor or its ligand to inhibit inflammatory signaling; and inhibition of downstream JAK-STAT signaling to treat myeloid malignancies.
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