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Published online before print December 20, 2005
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,1
* Medical Clinic, Uster Hospital, Switzerland;
Medical Clinic B Research Unit and
Division of Hematology, Department of Medicine, University Hospital, Zürich, Switzerland; and
Clinical Research Division, Fred Hutchinson Cancer Research Center, Seattle, Washington
1 Correspondence: Medical Clinic B Research Unit, Department of Medicine, University Hospital of Zürich, CH-8091 Zürich, Switzerland. E-mail: klinsog{at}usz.unizh.ch
The hemoglobinhaptoglobin (HbHp) scavenger receptor CD163 is a monocyte/macrophage-restricted surface antigen, whose expression is strongly up-regulated by glucocorticoids. We have previously shown that CD163 is expressed by acute myeloid leukemia (AML) cells of monocytic lineage. Herein, we expand this finding by demonstrating constitutive and glucocorticoid-enhanced CD163 expression on French-American-British M4/M5 AML cells, and leukemic blasts of other AML subtypes and normal hematopoietic progenitor cells do not express CD163. We provide evidence that the functional characteristics of CD163 are preserved on malignant cells by showing the capability of types M4/M5 blast cells to internalize HbHp by a CD163-mediated mechanism. Together, our results identify CD163 as a potential target for therapeutic intervention. It is important that CD163 does not appear to be released from leukemic blasts under noninflammatory conditions, thus reducing the probability of off-target side-effects as a result of competitive binding of potential therapeutic ligands to nonmembrane-bound CD163.
Key Words: monocyte/macrophage hemoglobin-haptoglobin complex
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