Modulation of HLA-G Expression in Human Neural Cells after Neurotropic Viral Infections

Lafon, Monique; Préhaud, Christophe; Mégret, Françoise; Lafage, Mireille; Mouillot, Gaël; Roa, Michèle; Moreau, Philippe; Rouas‐Freiss, Nathalie; Carosella, Edgardo D.

doi:10.1128/jvi.79.24.15226-15237.2005

Cited by 115 publications

(98 citation statements)

References 81 publications

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“…HLA-G has been suggested to participate in the escape of viruses from the immune response generated by the nervous system. 40 We previously observed an increase of HLA-G transcripts in the brain of VEEV-exposed nonhuman primates, and we see it in the present study in the naïve or vaccine responders PBMCs but not in the vaccine nonresponder group. 19 its transcription activator (i.e., PF4 and USF1) and a natural killer receptor that recognizes MHC class Ia and Ib molecules (CD160) were among the top biomarkers for the vaccine nonresponder group.…”

Section: Discussionsupporting

confidence: 71%

Host responses to live-attenuated Venezuelan equine encephalitis virus (TC-83)

Erwin-Cohen¹,

Porter²,

Pittman³

et al. 2012

Human Vaccines & Immunotherapeutics

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Section: Discussionsupporting

confidence: 71%

Host responses to live-attenuated Venezuelan equine encephalitis virus (TC-83)

Erwin-Cohen¹,

Porter²,

Pittman³

et al. 2012

Human Vaccines & Immunotherapeutics

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“…Both are associated with 2 microglobulin [22]. HLA-G, which was originally thought to be present exclusively in the human placenta [23,24] has also been detected in brain and neural cells [25,26] including human neurons [8].…”

Section: Introductionmentioning

confidence: 99%

“…One such molecule, the Ligand of Fas, FasL, has been shown to be involved in the killing of migratory T cells into the nervous system (NS) in rabies virus (RABV) infection [2,3]. HLA-G, a non classical MHC molecule which expression in cells is up regulated following infection with human cytomegalovirus (HCMV), human immunodeficiency virus (HIV-1) and RABV could also contribute by a similar mechanism to the immunoevasion of these viruses [4][5][6][7][8]. In addition, HIV-1 and HCMV up regulate the expression of another non classical MHC class I molecule,…”

Section: Introductionmentioning

confidence: 99%

“…The question whether the HLA-E can be employed by neurons during infection of the NS by viruses which are known to escape the adverse host immune response such as RABV [2,3,8,27] or not such as latent strain of HSV-1 (KOS virus) was challenged here. We therefore investigated whether RABV and HSV-1 infected human neurons express HLA-E and whether HLA-E molecules reach the cell surface of the infected neurons.…”

Section: Introductionmentioning

confidence: 99%

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Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

et al. 2007

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Abbreviations : RABV (rabies virus), HSV-1 (herpes simplex virus type 1), mAb monoclonal antibody, HCMV ( Human cytomegalovirus) 2 Abstract HLA-G and E are non classical human MHC class I molecules. They may promote tolerance leading to virus and tumour immune escape. We recently described that the herpes simplex virus type 1 (HSV-1), a neurotropic virus inducing chronic infection and neuron latency, and rabies virus (RABV), a neuronotropic virus triggering acute neuron infection -up-regulate HLA-G expression in human neurons (NT2-N). Surface expression was only detected after RABV infection. We investigated here whether RABV and HSV-1 up regulate HLA-E expression in human neuronal precursors (Ntera-2D/1). We found that RABV and -not HSV-1-up regulates HLA-E expression, nevertheless HLA-E could not be detected on the surface of RABV infected Ntera-2D/1. Altogether these data suggest that HLA-G and not HLA-E could contribute to the immune escape of RABV. In contrast, there was no evidence that these molecules are used by latent HSV-1infection. Thus, neurotropic viruses that escape the host immune response totally (RABV) or partially (HSV-1) regulate HLA-G expression on human neuronal cells differentially.3

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“…One of the cytokines that is highly expressed in RPE cells is IFN-␤. Induction of Type 1 IFN gene expression is an essential component of innate immunity (22,23). Recent studies (24) have also shown that neurons produce high levels of IFN-␤ through TLR 3 signaling.…”

mentioning

confidence: 99%

IFN-β Provides Immuno-Protection in the Retina by Inhibiting ICAM-1 and CXCL9 in Retinal Pigment Epithelial Cells

Hooks

Nagineni

Hooper

et al. 2008

The Journal of Immunology

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The retinal pigment epithelial (RPE) cell is a potent regulatory cell that facilitates normal physiologic processes and plays a critical role in a variety of retinal diseases. We evaluated IFN-β production in human RPE cells through TLR signaling and investigated the effects of IFN-β on RPE cells. RPE cells treated with poly(I:C) or infected with an RNA virus produce IFN-β. Kinetic studies revealed that IFN-β levels continue to increase over a 48-h period and this was associated with the up-regulation of IRF-7 gene expression, a known positive feedback molecule for IFN-β production. Microarray analysis revealed that in IFN-β treated cells, 480 genes of 22,283 genes were up or down-regulated by >2-fold. We hypothesize that IFN-β induction during TLR signaling in the retina is an immunosuppressive factor produced to limit immunopathologic damage. Cytokine activation of RPE cells results in the production of the chemokines, CXCL9 and CXCL10, and the adhesion molecule, ICAM-1. Pretreatment of RPE cells with IFN-β resulted in inhibition of ICAM-1 production and elimination of CXCL9 production. This treatment did not alter CXCL10 production. Anti-IFN-β Ab blocked the inhibitory action of IFN-β. Real time PCR analysis revealed that IFN-β treatment inhibited gene expression of sICAM-1 and CXCL9. The results indicate a critical role for RPE cell derived IFN-β in the down-regulation of CXCL9 and ICAM-1 expression in the retina and suggest that the inhibition of CXCL9 is an immuno-suppressive mechanism that protects the retina from excessive inflammation.

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Modulation of HLA-G Expression in Human Neural Cells after Neurotropic Viral Infections

Abstract: HLA-G is

Cited by 115 publications

References 81 publications

Host responses to live-attenuated Venezuelan equine encephalitis virus (TC-83)

Host responses to live-attenuated Venezuelan equine encephalitis virus (TC-83)

Modulation of HLA-G and HLA-E Expression in Human Neuronal Cells After Rabies Virus or Herpes Virus Simplex Type 1 Infections

IFN-β Provides Immuno-Protection in the Retina by Inhibiting ICAM-1 and CXCL9 in Retinal Pigment Epithelial Cells

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