Inhibition of marrow CFU-E colony formation from human immunodeficiency virus-infected patients by beta- and gamma-interferon.
Increased production of cytokines such as beta-interferon (IFN) and gamma-IFN may contribute to the anemia frequently observed in patients with human immunodeficiency virus (HIV) infection. The hypothesis that HIV infection might enhance the susceptibility of erythroid progenitors to cytokine-mediated inhibition was evaluated by comparing the effects of beta- and gamma-IFN on in vitro colony formation by marrow erythroid colony-forming units (CFU-E) from HIV patients, normal volunteers, and anemic non-HIV-infected individuals. CFU-E colony formation from HIV patients was not significantly different from controls, and the degree of inhibition by IFN did not differ among patient subsets. HIV infection does not appear to impair baseline CFU-E colony formation, nor does it appear to enhance the susceptibility of CFU-E to suppression by cytokines.
Dallalio
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Hematology/Oncology Division, University of Cincinnati College of Medicine, Ohio, USA.
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D000740:Anemia / Q000473:pathology; D001853:Bone Marrow / Q000473:pathology*; D002478:Cells, Cultured; D003114:Colony-Forming Units Assay; D015658:HIV Infections / Q000473:pathology*; D006412:Hematopoietic Stem Cells / Q000473:pathology*; D006801:Humans; D016899:Interferon-beta / Q000494:pharmacology*; D007371:Interferon-gamma / Q000494:pharmacology*; D011994:Recombinant Proteins / Q000494:pharmacology
D011994:Recombinant Proteins; D016899:Interferon-beta; D007371:Interferon-gamma