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Verfasst von:Lahdou, Imad [VerfasserIn]   i
 Engler, Christoph [VerfasserIn]   i
 Mehrle, Stefan [VerfasserIn]   i
 Daniel, Volker [VerfasserIn]   i
 Sadeghi, Mahmoud [VerfasserIn]   i
 Opelz, Gerhard [VerfasserIn]   i
 Terness, Peter [VerfasserIn]   i
Titel:Role of human corneal endothelial cells in T-cell-mediated alloimmune attack in vitro
Verf.angabe:Imad Lahdou, Christoph Engler, Stefan Mehrle, Volker Daniel, Mahmoud Sadeghi, Gerhard Opelz, and Peter Terness
E-Jahr:2014
Jahr:March 2014
Umfang:9 S.
Fussnoten:Gesehen am 21.09.2021
Titel Quelle:Enthalten in: Investigative ophthalmology & visual science
Ort Quelle:Rockville, Md. : ARVO, 1977
Jahr Quelle:2014
Band/Heft Quelle:55(2014), 3 vom: März, Seite 1213-1221
ISSN Quelle:1552-5783
Abstract:Human corneal endothelial cells (HCEC) are a potential target of immune attack after corneal transplantation. The aim of this in vitro study was to investigate the role of HCEC during the alloimmune response of T-cells by examining cytokine profiles, function of the immunosuppressive enzyme indoleamine 2,3-dioxigenase (IDO), major histocompatibility complex (MHC-I/-II), T-cell proliferation, and the induction of cell death. Real-time PCR and RP-HPLC were used to determine IDO expression and activity. Multiplex assay was performed for quantification of cytokine levels. T-cell proliferation was assessed by thymidine incorporation, and HCEC cell death was measured by flow cytometry. Human corneal endothelial cells induce strong proliferation of allogeneic T-cells and an increase of proinflammatory cytokines such as interleukin-1α (IL-1α), IL-1β, IL-6, interferon-gamma (IFN-γ), and tumor necrosis factor-alpha (TNF-α). Tumor necrosis factor-alpha (and to a lesser extent IFN-γ) induces apoptosis. Moreover, IFN-γ strongly upregulates MHC-II molecules and IDO activity in HCEC as reflected by high kynurenine (Kyn) concentrations. Interestingly, the T-cell response was not affected by increased IDO activity, since blocking of IDO did not affect the proliferation rate. Indoleamine 2,3-dioxigenase-induced Kyn levels did not exceed concentrations of 175 ± 20 μM. Concentrations of ≥400 μM Kyn were required to suppress T-cell proliferation. Our data show that T-cell attack on HCEC leads to increased concentrations of proinflammatory cytokines. Inflammatory cytokines induce apoptosis and upregulate MHC-II molecules and IDO in HCEC. Although increased IDO activity does not influence the T-cell response, it constitutes an inflammatory marker of the alloimmune response toward HCEC.
DOI:doi:10.1167/iovs.13-11930
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Volltext ; Verlag ; Resolving-System: https://doi.org/10.1167/iovs.13-11930
 kostenfrei: Volltext: http://dx.doi.org/10.1167/iovs.13-11930
 DOI: https://doi.org/10.1167/iovs.13-11930
Datenträger:Online-Ressource
Sprache:eng
K10plus-PPN:1525061453
Verknüpfungen:→ Zeitschrift

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