title: Phenotypic and functional changes in peripheral blood monocytes during progression of human immunodeficiency virus infection. Effects of soluble immune complexes, cytokines, subcellular particulates from apoptotic cells, and HIV-1-encoded proteins on monocytes phagocytic function, oxidative burst, transendothelial migration, and cell surface phenotype.
abstract: We postulated that changes in the cell surface display of molecules that facilitate cell-cell and cell-matrix adhesions may reflect the changing immunosurveillance capacity of blood monocytes during progression of human immunodeficiency virus (HIV) infections. In Centers for Disease Control (CDC) stage A patients, whose monocytes' ability to phagocytose bacteria and generate reactive oxygen intermediates is often increased, the frequency of monocytes expressing CD49d, HLA-DP, HLA-DQ, and an activation epitope of CD11a/CD18 was increased and monocyte transendothelial migration was unimpaired. In CDC stage B/C patients, whose monocytes' ability to phagocytose bacteria and migrate across confluent endothelial monolayers was diminished, surface expression of CD49e and CD62L and the percentage of monocytes expressing CD18, CD11a, CD29, CD49e, CD54, CD58, CD31, and HLA-I were significantly decreased. Incubating normal donor monocytes with immune complexes in vitro reproduced the phenotypic and functional abnormalities seen in stage B/C patients. By contrast, in vitro stimulation with subcellular particulates released by apoptotic lymphocytes reproduced changes seen in stage A patients' monocytes. Although circulating monocytes appear to be activated at all stages, these data suggest that the high levels of circulating immune complexes, found predominantly in the later stages of HIV infection, may be particularly instrumental in reducing the monocyte's capacity to maintain surveillance against infection.
authors.affiliation: Research Center for AIDS and HIV-related Infections, Veterans Affairs Medical Center, Houston, Texas 77030, USA.
authors.forename: J
authors.initials: J
authors.lastname: Trial
authors.forename: H H
authors.initials: HH
authors.lastname: Birdsall
authors.forename: J A
authors.initials: JA
authors.lastname: Hallum
authors.forename: M L
authors.initials: ML
authors.lastname: Crane
authors.forename: M C
authors.initials: MC
authors.lastname: Rodriguez-Barradas
authors.forename: A L
authors.initials: AL
authors.lastname: de Jong
authors.forename: B
authors.initials: B
authors.lastname: Krishnan
authors.forename: C E
authors.initials: CE
authors.lastname: Lacke
authors.forename: C G
authors.initials: CG
authors.lastname: Figdor
authors.forename: R D
authors.initials: RD
authors.lastname: Rossen
mesh_terms: D000936:Antigen-Antibody Complex / Q000494:pharmacology; D015703:Antigens, CD / Q000032:analysis; D017209:Apoptosis / Q000502:physiology; D002465:Cell Movement; D003165:Complement System Proteins / Q000032:analysis; D016207:Cytokines / Q000494:pharmacology; D015658:HIV Infections / Q000145:classification* / Q000276:immunology*; D006680:HLA Antigens / Q000032:analysis; D006801:Humans; D007157:Immunologic Surveillance; D008214:Lymphocytes / Q000473:pathology; D008297:Male; D009000:Monocytes / Q000187:drug effects / Q000276:immunology* / Q000648:ultrastructure; D010587:Phagocytosis / Q000187:drug effects; D010641:Phenotype; D017382:Reactive Oxygen Species; D011948:Receptors, Antigen, T-Cell / Q000032:analysis; D014764:Viral Proteins / Q000494:pharmacology
chemical_list: D000936:Antigen-Antibody Complex; D015703:Antigens, CD; D016207:Cytokines; D006680:HLA Antigens; D017382:Reactive Oxygen Species; D011948:Receptors, Antigen, T-Cell; D014764:Viral Proteins; D003165:Complement System Proteins