Neutrophils aid in protection of the vaginal mucosae of immune mice against challenge with herpes simplex virus type 2.
about
Herpes simplex virus and the chemokines that mediate the inflammation.Modulation of immunity against herpes simplex virus infection via mucosal genetic transfer of plasmid DNA encoding chemokines.Role of CD28/CD80-86 and CD40/CD154 costimulatory interactions in host defense to primary herpes simplex virus infection.Estradiol regulates susceptibility following primary exposure to genital herpes simplex virus type 2, while progesterone induces inflammation.Vaccine-induced serum immunoglobin contributes to protection from herpes simplex virus type 2 genital infection in the presence of immune T cells.Interleukin-12 (IL-12) and IL-18 are important in innate defense against genital herpes simplex virus type 2 infection in mice but are not required for the development of acquired gamma interferon-mediated protective immunity.RNA-dependent protein kinase is required for alpha-1 interferon transgene-induced resistance to genital herpes simplex virus type 2.Tannic acid modified silver nanoparticles show antiviral activity in herpes simplex virus type 2 infectionProphylactic and therapeutic modulation of innate and adaptive immunity against mucosal infection of herpes simplex virusClearance of herpes simplex virus type 2 by CD8+ T cells requires gamma interferon and either perforin- or Fas-mediated cytolytic mechanismsProtective effect of avian myelomonocytic growth factor in infection with Marek's disease virusLoss of the type I interferon pathway increases vulnerability of mice to genital herpes simplex virus 2 infection.Cervico-vaginal immunoglobulin G levels increase post-ovulation independently of neutrophils.Mucosal administration of CpG oligodeoxynucleotide elicits strong CC and CXC chemokine responses in the vagina and serves as a potent Th1-tilting adjuvant for recombinant gD2 protein vaccination against genital herpesNP-1, a rabbit alpha-defensin, prevents the entry and intercellular spread of herpes simplex virus type 2HSV-2 regulates monocyte inflammatory response via the Fas/FasL pathwayKaposi's sarcoma-associated herpesvirus infection of endothelial cells inhibits neutrophil recruitment through an interleukin-6-dependent mechanism: a new paradigm for viral immune evasionInduction of innate immunity against herpes simplex virus type 2 infection via local delivery of Toll-like receptor ligands correlates with beta interferon production.Local delivery of CpG oligodeoxynucleotides induces rapid changes in the genital mucosa and inhibits replication, but not entry, of herpes simplex virus type 2.Early resolution of herpes simplex virus type 2 infection of the murine genital tract involves stimulation of genital parenchymal cells by gamma interferonSusceptibility of CCR5-deficient mice to genital herpes simplex virus type 2 is linked to NK cell mobilizationDistinct Upstream Role of Type I IFN Signaling in Hematopoietic Stem Cell-Derived and Epithelial Resident Cells for Concerted Recruitment of Ly-6Chi Monocytes and NK Cells via CCL2-CCL3 CascadeModulation of Female Genital Tract-Derived Dendritic Cell Migration and Activation in Response to Inflammatory Cytokines and Toll-Like Receptor AgonistsComparison of the host immune response to herpes simplex virus 1 (HSV-1) and HSV-2 at two different mucosal sites.Antibody-mediated protection against genital herpes simplex virus type 2 disease in mice by Fc gamma receptor-dependent and -independent mechanisms.Effector CD4+ T-cell involvement in clearance of infectious herpes simplex virus type 1 from sensory ganglia and spinal cordsAntiviral immune responses in the genital tract: clues for vaccines.Herpes simplex virus type 2-induced mortality following genital infection is blocked by anti-tumor necrosis factor alpha antibody in CXCL10-deficient mice.Chemokines and Chemokine Receptors Critical to Host Resistance following Genital Herpes Simplex Virus Type 2 (HSV-2) InfectionCXCR3 deficiency increases susceptibility to genital herpes simplex virus type 2 infection: Uncoupling of CD8+ T-cell effector function but not migration.Neutrophils recruited by IL-22 in peripheral tissues function as TRAIL-dependent antiviral effectors against MCMV.Involvement of intracellular free Ca2+ in enhanced release of herpes simplex virus by hydrogen peroxide.Differential polarization of immune responses by genetic cotransfer of chemokines changes the protective immunity of DNA vaccine against pseudorabies virus.The lack of RNA-dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infection.
P2860
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P2860
Neutrophils aid in protection of the vaginal mucosae of immune mice against challenge with herpes simplex virus type 2.
description
1999 nî lūn-bûn
@nan
1999 թուականի Օգոստոսին հրատարակուած գիտական յօդուած
@hyw
1999 թվականի օգոստոսին հրատարակված գիտական հոդված
@hy
1999年の論文
@ja
1999年論文
@yue
1999年論文
@zh-hant
1999年論文
@zh-hk
1999年論文
@zh-mo
1999年論文
@zh-tw
1999年论文
@wuu
name
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@ast
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@en
type
label
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@ast
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@en
prefLabel
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@ast
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@en
P2860
P1433
P1476
Neutrophils aid in protection ...... h herpes simplex virus type 2.
@en
P2093
G N Milligan
P2860
P304
P577
1999-08-01T00:00:00Z