Abstract
We have previously demonstrated impaired monocytic function after HIV-1 infection in human macrophage hybridoma cell lines including an inability to present soluble antigen to T cells. To further clarify this defect, we infected human macrophage hybridomas and primary monocytes for varying peroids of time with HIV- Inm and HIV- IB.L respectively and evaluated their ability to take up antigens by laser confocal microscopy. HIV-1 infected and uninfected human macrophage hybridoma cell lines and primary monocytes were pulsed with FTTC-labeled tetanus toxoid (TT). FITC-labeled keyhole limpet hemocyànin (KLH), and FITC-labeled ovalbumin (OVA) for 0 minutes, 15 minutes, 30 minutes, and 60 minutes. Intracellular punctate fluorescence staining was evident at IS minutes with all three FITC-labeled antigens in the uninfected macrophage hybridoma cell lines and primary monocytes. However, 5 days after HTV- IBU. infection of the primary monocytes and 2 weeks after HlV-lms infection of the macrophage hybridoma cell lines, there was a marked decrease in uptake of all three antigens at all time points tested. Immune complexes of FITC-labeled TT and anti-TT antibodies were internalized in both HIV-1 infected and uninfected cells suggesting that Fc receptor mediated uptake was intact. In order to dissect out the level of the antigen processing defect we attempted to co-localize the FITC-labeled antigens with early endosomal markers (antiM6PR), Class n (anti-DR), and late endosomal markers (DAMP). In the uninfected cells die FITC-labeled antigens co-localized with DAMP, DR and M6PR while in the HTV-1 infected cells there was no co-localization. Our data suggest that antigen trafficking is impaired in HIV-1 monocytic cells.
Original language | English |
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Pages (from-to) | A1021 |
Journal | FASEB Journal |
Volume | 10 |
Issue number | 6 |
State | Published - 1996 |