Coreceptor/chemokine receptor expression on human hematopoietic cells: biological implications for human immunodeficiency virus-type 1 infection.

摘要: The recent discovery of chemokine receptors as coreceptors for human immunodeficiency virus–type 1 (HIV-1) entry offers new avenues investigating the pathogenesis acquired syndrome (AIDS)-related cytopenias. To this end, we sought to (1) phenotype hematopoietic cells CD4 and HIV-1 CXCR4, CCR5, CCR3, CCR2b; (2) correlate receptor expression with their susceptibility infection; (3) examine any potential interplay between inflammatory cytokines released during infection regulation expression. Fluorescence-activated cell sorting (FACS) analysis bone marrow mononuclear (BMMNC), derived from serum-free expanded lineages (colony-forming unit–granulocyte-macrophage [CFU-GM], colony-forming unit-megakaryocyte [CFU-Meg], burst-forming unit-erythroid [BFU-E]), CD34+ showed differential some lineage specificity. Significantly, FACS-sorted CXCR4+/CD34+ had same clonogeneic CXCR4−/CD34+ cells. Reverse transcriptase-polymerase chain reaction (RT-PCR) candidate stem (HSC; CD34+, c-kit+, Rho123low) presence CXCR4 mRNA but not mRNA. Infection studies Env-pseudotyped luciferase reporter viruses indicated that X4 Env (CXCR4-using) pseudotypes infected megakaryocytic cells, whereas R5 (CCR5-using) did not. Similarly, granulocyte-macrophage in a CD4/CCR5-dependent manner. Erythroid were resistant or viral infection. Finally, found γ-interferon treatment upregulated on primary In summary, delineation is first step towards dissecting chemokine-chemokine axes may play role proliferation homing. Furthermore, likely be more complicated than mere physical cognate receptor. Lastly, our results suggest secretion