B7‐H1 (CD274) inhibits the development of herpetic stromal keratitis (HSK)

Hashimoto, Jun; Seo, Su K.; Jeong, Hye Young; Seo, Hyoun Mi; Zhu, Gefeng; Chen, Lieping; Choi, In Taek

doi:10.1016/j.febslet.2005.09.098

Cited by 37 publications

(39 citation statements)

References 28 publications

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“…The PD-1 pathway is involved in the development of T cell tolerance and has been implicated in the persistence of a variety of chronic viral infections, including lymphocytic choriomeningitis virus, HIV, HBV, and hepatitis C virus (37)(38)(39)(40)(41)(42)(43)(44). There is already some evidence that blockade of the PD-1/programmed death ligand-1 synapse could alter the balance between cytolytic and noncytolytic CD8 + effector T cell functions, resulting in exacerbation of immune-mediated tissue damage in herpetic keratitis or in autoimmune enteritis (45,46). It is possible that the PD-1 pathway acts as a mechanism by which CD8 + T cells engage in cross-talk with the target cells to program their effector functions; the hypothesis that the PD-1 pathway may have a role in modulating the effector functions of virus-specific CD8 + T cells deserves to be investigated in future studies.…”

Section: Discussionmentioning

confidence: 99%

CD8+ T Cell Control of Hepatitis B Virus Replication: Direct Comparison between Cytolytic and Noncytolytic Functions

Phillips

Chokshi

Riva

et al. 2009

The Journal of Immunology

195

157

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Resolution of hepatitis B virus (HBV) infection was believed to be attributed to the cytotoxic T cell–mediated killing of infected hepatocytes. However, studies in HBV transgenic mice and HBV-infected chimpanzees revealed that T cell control of HBV replication also involves cytokine-mediated noncytolytic mechanisms. The relative role of cytolytic and noncytolytic functions of virus-specific CD8+ T cells during interaction with HBV-producing hepatocytes is not well understood. By using HLA-A2 matched effector cells (CD8+ T cell line or clone) and target cells supporting full HBV replication, we demonstrate that virus-specific CD8+ T cells can inhibit HBV replication in HBV-producing hepatocytes with minimal cell lysis. Although CD8+ T cells kill a fraction of infected cells, this effect is minimal, and most of the viral inhibition is mediated by noncytolytic mechanisms. CD8+ T cells produce an array of cytokines, among which IFN-γ and TNF-α are responsible for HBV inactivation in the target cells. Blockade of IFN-γ and TNF-α abrogated the noncytolytic inhibition of HBV, indicating that these two cytokines mediate the control of HBV by noncytolytic mechanisms. Furthermore, treatment of the HBV-producing hepatocytes with rIFN-γ and rTNF-α resulted in an efficient suppression of viral replication without cytotoxicity. In contrast, coculture of the same target cells with activated HLA-mismatched mitogen-activated lymphomononuclear cells caused a marked cytolytic effect and was less effective in HBV control. These results provide direct evidence that virus-specific CD8+ T cells efficiently control HBV replication by noncytolytic mechanisms, and this effect is mediated by IFN-γ and TNF-α.

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Section: Discussionmentioning

confidence: 99%

CD8+ T Cell Control of Hepatitis B Virus Replication: Direct Comparison between Cytolytic and Noncytolytic Functions

Phillips

Chokshi

Riva

et al. 2009

The Journal of Immunology

195

157

View full text Add to dashboard Cite

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“…Accordingly, several groups have demonstrated that blocking PD-1:PD-Ls interactions in vitro reverses the exhaustion of HIV and hepatitis C virus-specific CD8 ϩ and CD4 ϩ T cells and restores cytokine production and proliferation (36, 38, 56, 57). Moreover, administration of PD-L1-specific blocking mAbs leads to exacerbated keratitis-increased HSV-specific effector CD4 ϩ T cell proliferation, IFN-␥ production, and survival, suggesting that PD-L1 may participate in limiting immune-mediated tissue damage in herpes stromal keratitis infection (58). Besides, during hepatitis B virus infection, PD-1:PD-L1 interactions were shown to contribute to the suppression of IFN-␥ secretion following Ag recognition in the liver (59).…”

Section: Discussionmentioning

confidence: 99%

Programmed Death (PD)-1:PD-Ligand 1/PD-Ligand 2 Pathway Inhibits T Cell Effector Functions during Human Tuberculosis

Jurado

Alvarez

Pasquinelli

et al. 2008

The Journal of Immunology

234

216

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Protective immunity against Mycobacterium tuberculosis requires the generation of cell-mediated immunity. We investigated the expression and role of programmed death 1 (PD-1) and its ligands, molecules known to modulate T cell activation, in the regulation of IFN-γ production and lytic degranulation during human tuberculosis. We demonstrated that specific Ag-stimulation increased CD3+PD-1+ lymphocytes in peripheral blood and pleural fluid from tuberculosis patients in direct correlation with IFN-γ production from these individuals. Moreover, M. tuberculosis-induced IFN-γ participated in the up-regulation of PD-1 expression. Blockage of PD-1 or PD-1 and its ligands (PD-Ls: PD-L1, PD-L2) enhanced the specific degranulation of CD8+ T cells and the percentage of specific IFN-γ-producing lymphocytes against the pathogen, demonstrating that the PD-1:PD-Ls pathway inhibits T cell effector functions during active M. tuberculosis infection. Furthermore, the simultaneous blockage of the inhibitory receptor PD-1 together with the activation of the costimulatory protein signaling lymphocytic activation molecule led to the promotion of protective IFN-γ responses to M. tuberculosis, even in patients with weak cell-mediated immunity against the bacteria. Together, we demonstrated that PD-1 interferes with T cell effector functions against M. tuberculosis, suggesting that PD-1 has a key regulatory role during the immune response of the host to the pathogen.

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“…ϩ dendritic cells, in conjunction with increased viral load (23); in another study, monoclonal antibody blockade of PD-L1 resulted in decreased apoptosis and increased proliferation and IFN-␥ secretion by HSV-1-specific CD4 T cells, which exasperated herpetic stromal keratitis (24).…”

Section: Cells and Pd-l1mentioning

confidence: 99%

Varicella-Zoster Virus Downregulates Programmed Death Ligand 1 and Major Histocompatibility Complex Class I in Human Brain Vascular Adventitial Fibroblasts, Perineurial Cells, and Lung Fibroblasts

Jones

Blackmon

Neff

et al. 2016

J Virol

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V aricella-zoster virus (VZV) is a common, neurotropic DNA alphaherpesvirus that causes varicella (chickenpox) upon primary infection, after which virus becomes latent in ganglionic neurons along the entire neuraxis (1-6). With a decline in VZVspecific cell-mediated immunity, VZV reactivates in elderly or immunocompromised individuals, most commonly causing zoster (shingles). VZV can also reactivate and spread transaxonally to cerebral arteries to produce stroke with or without rash (VZV vasculopathy). Recent studies show that aside from stroke, VZV vasculopathy presents as giant cell arteritis, which is the most common cause of systemic vasculitis in the elderly (7), as well as granulomatous aortitis (8).Studies of VZV-infected cerebral and temporal arteries from patients with VZV vasculopathy show viral antigen predominantly in the outermost adventitia in early infection, supporting deposition of virus from nerve fibers that terminate within this layer followed by transmural spread (7, 9). Persistent inflammation with a predominance of T cells and macrophages can be seen even up to 10 months after disease onset and is associated with pathological vascular remodeling (10). The mechanism(s) by which inflammatory cells persist to cause vascular damage in VZV-infected arteries is unknown.Programmed cell death ligand 1 (PD-L1), a 40-kDa type 1 transmembrane protein in the B7 immunoglobulin family that can be expressed on virtually all nucleated cells (11), suppresses the immune system through interaction with its receptor, pro-

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B7‐H1 (CD274) inhibits the development of herpetic stromal keratitis (HSK)

Cited by 37 publications

References 28 publications

CD8+ T Cell Control of Hepatitis B Virus Replication: Direct Comparison between Cytolytic and Noncytolytic Functions

CD8+ T Cell Control of Hepatitis B Virus Replication: Direct Comparison between Cytolytic and Noncytolytic Functions

Programmed Death (PD)-1:PD-Ligand 1/PD-Ligand 2 Pathway Inhibits T Cell Effector Functions during Human Tuberculosis

Varicella-Zoster Virus Downregulates Programmed Death Ligand 1 and Major Histocompatibility Complex Class I in Human Brain Vascular Adventitial Fibroblasts, Perineurial Cells, and Lung Fibroblasts

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