共 41 条
GB Virus C Particles Inhibit T Cell Activation via Envelope E2 Protein-Mediated Inhibition of TCR Signaling
被引:32
作者:

Bhattarai, Nirjal
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机构:
Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
Univ Iowa, Interdisciplinary Program Mol & Cellular Biol, Iowa City, IA 52242 USA
Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA

McLinden, James H.
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h-index: 0
机构:
Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA

Xiang, Jinhua
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h-index: 0
机构:
Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA

Landay, Alan L.
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h-index: 0
机构:
Rush Univ, Med Ctr, Chicago, IL 60612 USA Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA

Chivero, Ernest T.
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h-index: 0
机构:
Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
Univ Iowa, Interdisciplinary Program Mol & Cellular Biol, Iowa City, IA 52242 USA Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA

Stapleton, Jack T.
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h-index: 0
机构:
Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
Univ Iowa, Interdisciplinary Program Mol & Cellular Biol, Iowa City, IA 52242 USA
Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA
Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
机构:
[1] Iowa City Vet Affairs Med Ctr, Iowa City, IA 52242 USA
[2] Univ Iowa, Interdisciplinary Program Mol & Cellular Biol, Iowa City, IA 52242 USA
[3] Univ Iowa, Dept Internal Med, Iowa City, IA 52242 USA
[4] Rush Univ, Med Ctr, Chicago, IL 60612 USA
[5] Univ Iowa, Dept Microbiol, Iowa City, IA 52242 USA
基金:
美国国家卫生研究院;
关键词:
HIV-INFECTED INDIVIDUALS;
ANTIRETROVIRAL THERAPY;
IMMUNE ACTIVATION;
VIRAL LOAD;
EXOSOMES;
SURVIVAL;
VIREMIA;
BIND;
RNA;
REPLICATION;
D O I:
10.4049/jimmunol.1300589
中图分类号:
R392 [医学免疫学];
Q939.91 [免疫学];
学科分类号:
100102 ;
摘要:
Viruses enter into complex interactions within human hosts, leading to facilitation or suppression of each other's replication. Upon coinfection, GB virus C (GBV-C) suppresses HIV-1 replication in vivo and in vitro, and GBV-C coinfection is associated with prolonged survival in HIV-infected people. GBV-C is a lymphotropic virus capable of persistent infection. GBV-C infection is associated with reduced T cell activation in HIV-infected humans, and immune activation is a critical component of HIV disease pathogenesis. We demonstrate that serum GBV-C particles inhibited activation of primary human T cells. T cell activation inhibition was mediated by the envelope glycoprotein E2, because expression of E2 inhibited TCR-mediated activation of Lck. The region on the E2 protein was characterized and revealed a highly conserved peptide motif sufficient to inhibit TCR-mediated signaling. The E2 region contained a predicted Lck substrate site, and substitution of an alanine or histidine for the tyrosine reversed TCR-signaling inhibition. GBV-C E2 protein and a synthetic peptide representing the inhibitory amino acid sequence were phosphorylated by Lck in vitro. The synthetic peptide also inhibited TCR-mediated activation of primary human CD4(+) and CD8(+) T cells. Extracellular microvesicles from GBV-C E2-expressing cells contained E2 protein and inhibited TCR signaling in bystander T cells not expressing E2. Thus, GBV-C reduced global T cell activation via competition between its envelope protein E2 and Lck following TCR engagement. This novel inhibitory mechanism of T cell activation may provide new approaches for HIV and immunoactivation therapy.
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页码:6351 / 6359
页数:9
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