Chronically HIV-1-infected monocytic cells induce apoptosis in cocultured T cells.

Chen, Houchu; Yip, Y. K.; George, Ilena C.; Tyorkin, Max; Salik, Erez; Sperber, Kirk

doi:10.4049/jimmunol.175.12.8443

Cited by 12 publications

(12 citation statements)

References 69 publications

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“…The cells were then washed in ice-cold PBS, centrifuged at 500 g at 4°C, and then incubated with annexin V-FITC at room temperature for 10 min in the dark. The cells were analyzed by flow cytometry to measure the annexin V-positive population, gating on the live cells (7).…”

Section: Generationmentioning

confidence: 99%

Accessory cell function of airway epithelial cells

Oei

Kalb²,

Beuria³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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Oei, Erwin, Thomas Kalb, Prarthana Beuria, Matthieu Allez, Atsushi Nakazawa, Miyuki Azuma, Michael Timony, Zanetta Stuart, Houchu Chen, and Kirk Sperber. Accessory cell function of airway epithelial cells.We previously demonstrated that airway epithelial cells (AECs) have many features of accessory cells, including expression of class II molecules CD80 and CD86 and functional Fcγ receptors. We have extended these studies to show that freshly isolated AECs have mRNA for cathepsins S, V, and H [proteases important in antigen (Ag) presentation], invariant chain, human leukocyte antigen (HLA)-DM-α and HLA-DM-β, and CLIP, an invariant chain breakdown product. A physiologically relevant Ag, ragweed, was colocalized with HLA-DR in AECs, and its uptake was increased by granulocyte-macrophage colony-stimulating factor and IFN-γ treatments, which had no effect on CD80 and CD86 expression. We demonstrate the presence of other costimulatory molecules, including B7h and B7-H1, on AECs and the increased expression of B7-H1 on AECs after treatment with granulocyte-macrophage colony-stimulating factor and IFN-γ. Finally, we compared T cell proliferation after allostimulation with AECs and dendritic cells (DCs). The precursor frequency of peripheral blood T cells responding to AECs was 0.264% compared with 0.55% for DCs. DCs stimulated CD45RO+, CD45RA+, CCR7+and CCR7−CD4+, and CD8+T cells, whereas AECs stimulated only CD45RO+, CD45RA−, CCR7−, CD4+, and CD8+T cells. There was no difference in cytokine production, type of memory T cells stimulated (effector vs. long-term memory), or apoptosis by T cells cocultured with AECs and DCs. The localization of AECs exposed to the external environment may make them important in the regulation of local immune responses.

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Section: Generationmentioning

confidence: 99%

Accessory cell function of airway epithelial cells

Oei

Kalb²,

Beuria³

et al. 2004

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…EtOH induces secretion of anti-inflammatory factors (transforming growth factor b and prostaglandin E 2 ) [1,11,12]. Acute EtOH intoxication can also suppress inflammatory responses in normal subjects through inhibition of accessory function and leukocyte migration [10,[13][14][15]. In simian immunodeficiency virus (SIV)-infected animals EtOH suppresses TNF-a and leads to increased susceptibility to secondary infections [16].…”

Section: Introductionmentioning

confidence: 99%

Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune function during disease

Haorah

Heilman

Diekmann

et al. 2004

Cellular Immunology

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Proteasomes (proteinase complexes, PR) and immunoproteasomes (IPR) degrade damaged proteins and affect protein processing required for antigen presentation by mononuclear phagocytes. These critical immune processes are attenuated during progressive HIV-1 infection and are affected by alcohol abuse. To investigate the mechanisms underlying these functional changes, we measured PR and CYP2E1 activities [an ethanol (EtOH) metabolizing enzyme] and reactive oxygen species (ROS) in human monocyte-derived macrophages (MDM) following HIV-1 infection and EtOH treatment. We observed progressive declines of PR activity and PR/IPR contents in HIV-1-infected MDM. PR activity and IPR expression increased after IFN-c stimulation but reduced after HIV-1 infection. EtOH inhibited both IFN-c-induced PR and IPR. Paradoxically, EtOH attenuated PR catalytic activity in infected MDM and suppressed viral replication. Elevated ROS followed EtOH exposure and paralleled decreased PR activity. The latter was restored by anti-oxidant. The data support the notion that HIV-1 infection and EtOH may work in concert to affect immune function including antigen presentation and thereby affect disease progression.

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“…These are experiments with four different T-cell donors. Columns: 1, T cells alone (T); 2, T ϩ HB-2; 3, T ϩ HB-2 HIV ; 4, T ϩ HB-2 HIV ϩ ddI; 5, T ϩ HB-2 HIV ϩ IDV; 6, T ϩ HB-2 HIV ϩIDV ϩ ddI; 7, T ϩ HB-2 HIV ϩ 5145; 8, T ϩ HB-2 HIV ϩ anti-IL-10; 9, T ϩ HB-2 HIV ϩ anti-IL-10 ϩ 5145; 10, T ϩ HB-2 HIV ϩ ddI, IDV, anti-IL-10, and 5145. clonal anti-gp120 antibody 5145 (10 g/ml) and repeated the MLR (17). Compared to the uninfected HB-2 cells, the 5145 antibodies partially restored T-cell proliferation in the HB-2 HIV cocultures (Fig.…”

Section: Effect Of Antiretroviral Therapy and Anti-gp120 Antibodies Omentioning

confidence: 99%

“…RosetteSep is a rapid, easy cell separation kit for the isolation of highly purified CD3 CD45RA A multiplicity of infection of 1 was used to infect the HB-2 cells with both HIV IIIB and HIV BaL for 90 min at 37°C, followed by three PBS washes and culture in CM (57). The cells were stained intracytoplasmically to determine the presence of HIV-1 proteins as described above (17). The p24 antigen levels in the culture supernatants were measured at day 5 according to manufacturers' protocol by using a commercial antigen capture enzyme-linked immunosorbent assay (ELISA; Dupont, Wilmington, Del.)…”

Section: Generationmentioning

confidence: 99%

“…For intracytoplasmic staining, cells were fixed and permeabilized with 70% ethanol for 30 min at 4°C. The cells were then washed three times with PBS, and the 5145 polyclonal human anti-HIV-1 antibodies (17) or control human antibodies were added for 30 min at 4°C, followed by affinitypurified FITC-conjugated goat anti-human immunoglobulin antibodies (Tago, Burlingame, Calif.), and then analyzed as described above. Our laboratory has routinely used 70% ethanol to permeabilize cells for intracytoplasmic staining (17,39,54).…”

Section: Generationmentioning

confidence: 99%

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Impaired Accessory Cell Function in a Human Dendritic Cell Line after Human Immunodeficiency Virus Infection

Beuria

Chen

Timoney

et al. 2005

Clin Vaccine Immunol

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We generated human dendritic cell (DC) hybridoma cell lines by fusing HGPRT-deficient promonocytic U937 cells with immature DCs obtained by culturing peripheral blood monocytes with interleukin-4 (IL-4; 1,000 U/ml) and granulocyte-macrophage colony-stimulating factor (100 U/ml) for 7 days and mature DCs by treatment with tumor necrosis factor alpha (12.5 g/ml) for 3 days. Only one fusion with immature DCs was successful and yielded four cell lines-HB-1, HB-2, HB-3, and HB-9-with an overall fusion efficiency of 0.0015%. The cell lines were stable in long-term culture, displayed morphological features typical of DCs, and expressed distinct class I and class II molecules not present on U937 (A*031012, B*51011, Cw*0701, DRB3*01011 52, and DR5*01011). A representative cell line, HB-2, that expressed DC markers including CD83, CD80 and CD86 could be induced to produce IL-12 through CD40 stimulation. After human immunodeficiency virus (HIV) infection, there was impairment of antigen-presenting cell (APC) function, which was manifested by an inability to stimulate allogeneic T-cell responses. There was no change in expression of major histocompatibility complex class I and class II antigens, CD83, CD40, CD4, CD11c, CD80, CD86, CD54, and CD58, or IL-12 production in the HIV-infected HB-2 cells. The HIV-infected HB-2 cells induced T-cell apoptosis in the cocultures. T-cell proliferation could be partially restored by using ddI, indinivir, and blocking anti-gp120 and anti-IL-10 antibodies. Our data suggest that there are multiple mechanisms that DCs use to inhibit T-cell responses in HIV-infected patients. The HB-2 cell line could be a useful model system to study APC function in HIV-infected DCs.

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Chronically HIV-1-infected monocytic cells induce apoptosis in cocultured T cells.

Abstract: Chronic ethanol ingestion in rats decreases granulocyte-macrophage colony-stimulating factor receptor expression and downstream signaling in the alveolar macrophage.

Cited by 12 publications

References 69 publications

Accessory cell function of airway epithelial cells

Accessory cell function of airway epithelial cells

Alcohol and HIV decrease proteasome and immunoproteasome function in macrophages: implications for impaired immune function during disease

Impaired Accessory Cell Function in a Human Dendritic Cell Line after Human Immunodeficiency Virus Infection

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