Herpes simplex virus-specific CD8+ T cells can clear established lytic infections from skin and nerves and can partially limit the early spread of virus after cutaneous inoculation.
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The role of dendritic cells in immunity against primary herpes simplex virus infectionsSkin CD4(+) memory T cells exhibit combined cluster-mediated retention and equilibration with the circulation.Distinct APC subtypes drive spatially segregated CD4+ and CD8+ T-cell effector activity during skin infection with HSV-1Persistence of skin-resident memory T cells within an epidermal niche.DOCK8 regulates lymphocyte shape integrity for skin antiviral immunityType I IFN suppresses Cxcr2 driven neutrophil recruitment into the sensory ganglia during viral infection.Immunization with a dominant-negative recombinant Herpes Simplex Virus (HSV) type 1 protects against HSV-2 genital disease in guinea pigs.A herpes simplex virus 2 (HSV-2) glycoprotein D-expressing nonreplicating dominant-negative HSV-2 virus vaccine is superior to a gD2 subunit vaccine against HSV-2 genital infection in guinea pigsInterleukin-36β provides protection against HSV-1 infection, but does not modulate initiation of adaptive immune responsesLytic gene expression is frequent in HSV-1 latent infection and correlates with the engagement of a cell-intrinsic transcriptional responsebeta-Glucan oligosaccharide enhances CD8(+) T cells immune response induced by a DNA vaccine encoding hepatitis B virus core antigen.Prophylactic and therapeutic modulation of innate and adaptive immunity against mucosal infection of herpes simplex virusLatent infection with herpes simplex virus is associated with ongoing CD8+ T-cell stimulation by parenchymal cells within sensory gangliaAge-related dysregulation of CD8+ T cell memory specific for a persistent virus is independent of viral replicationInflation and long-term maintenance of CD8 T cells responding to a latent herpesvirus depend upon establishment of latency and presence of viral antigens.Entry of herpes simplex virus type 1 (HSV-1) into the distal axons of trigeminal neurons favors the onset of nonproductive, silent infectionIntravaginal Zinc Oxide Tetrapod Nanoparticles as Novel Immunoprotective Agents against Genital Herpes.Development of a glycoprotein D-expressing dominant-negative and replication-defective herpes simplex virus 2 (HSV-2) recombinant viral vaccine against HSV-2 infection in miceEstablishment of HSV1 latency in immunodeficient mice facilitates efficient in vivo reactivation.Innate lymphotoxin receptor mediated signaling promotes HSV-1 associated neuroinflammation and viral replication.Delayed control of herpes simplex virus infection and impaired CD4(+) T-cell migration to the skin in mouse models of DOCK8 deficiencyA genital tract peptide epitope vaccine targeting TLR-2 efficiently induces local and systemic CD8+ T cells and protects against herpes simplex virus type 2 challengeLong-lived epithelial immunity by tissue-resident memory T (TRM) cells in the absence of persisting local antigen presentation.Reading the viral signature by Toll-like receptors and other pattern recognition receptors.Maintenance of T cell function in the face of chronic antigen stimulation and repeated reactivation for a latent virus infection.CD8+ T cells suppress viral replication in the cornea but contribute to VEGF-C-induced lymphatic vessel genesis.Lytic Promoters Express Protein during Herpes Simplex Virus Latency.IFN-α-driven CCL2 production recruits inflammatory monocytes to infection site in mice.Replication-defective virus vaccine-induced protection of mice from genital herpes simplex virus 2 requires CD4 T cellsThe immune response to herpes simplex virus type 1 infection in susceptible mice is a major cause of central nervous system pathology resulting in fatal encephalitis.Gender-dependent HLA-DR-restricted epitopes identified from herpes simplex virus type 1 glycoprotein D.Cutting edge: recombinant Listeria monocytogenes expressing a single immune-dominant peptide confers protective immunity to herpes simplex virus-1 infection.Loss of mandibular lymph node integrity is associated with an increase in sensitivity to HSV-1 infection in CD118-deficient miceCD4+ T cells are required for the priming of CD8+ T cells following infection with herpes simplex virus type 1.Selected Toll-like receptor ligands and viruses promote helper-independent cytotoxic T cell priming by upregulating CD40L on dendritic cells.Dendritic cell-based vaccines in treating recurrent herpes labialis: Results of pilot clinical study.Defense against HSV-1 in a murine model is mediated by iNOS and orchestrated by the activation of TLR2 and TLR9 in trigeminal ganglia.Neutrophils are dispensable in the modulation of T cell immunity against cutaneous HSV-1 infection.Dendritic cell subsets in primary and secondary T cell responses at body surfaces.Critical role of microRNA-155 in herpes simplex encephalitis
P2860
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P2860
Herpes simplex virus-specific CD8+ T cells can clear established lytic infections from skin and nerves and can partially limit the early spread of virus after cutaneous inoculation.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年学术文章
@wuu
2004年学术文章
@zh
2004年学术文章
@zh-cn
2004年学术文章
@zh-hans
2004年学术文章
@zh-my
2004年学术文章
@zh-sg
2004年學術文章
@yue
2004年學術文章
@zh-hant
name
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@en
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@nl
type
label
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@en
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@nl
prefLabel
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@en
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@nl
P2093
P1476
Herpes simplex virus-specific ...... s after cutaneous inoculation.
@en
P2093
Allison van Lint
Francis R Carbone
Margaret Ayers
Richard M Coles
P304
P356
10.4049/JIMMUNOL.172.1.392
P407
P577
2004-01-01T00:00:00Z