Literature DB >> 2783720

T lymphocytes in genital lymph nodes protect mice from intravaginal infection with herpes simplex virus type 2.

M R McDermott1, C H Goldsmith, K L Rosenthal, L J Brais.   

Abstract

Herpes simplex virus type 2 (HSV-2) is a human venereal pathogen that causes lethal neurological illness after intravaginal inoculation into BALB/cJ mice. Intravaginal vaccination of mice with an attenuated strain of HSV-2 rapidly induces immunity to a lethal intravaginal challenge with wild-type HSV-2. This resistance is transferrable to syngeneic mice with genital lymph node (GLN) cells but not with cells from other lymphoid sources. Here we demonstrate that minimal numbers of HSV-2-stimulated GLN T lymphocytes are required for resistance to genital infection by HSV-2 and that such cells migrate preferentially into HSV-2-infected genital tissue. Furthermore, the results suggest that HSV-2-specific cytotoxic T lymphocytes from the GLN may be one effector cell population participating locally in genital immunity to the virus. These findings indicate that mucosal immunity to genital HSV-2 infection requires the antigen stimulation of migratory T cells in the GLN.

Entities:  

Mesh:

Year:  1989        PMID: 2783720     DOI: 10.1093/infdis/159.3.460

Source DB:  PubMed          Journal:  J Infect Dis        ISSN: 0022-1899            Impact factor:   5.226


  25 in total

1.  The lack of RNA-dependent protein kinase enhances susceptibility of mice to genital herpes simplex virus type 2 infection.

Authors:  Daniel J J Carr; Todd Wuest; Lisa Tomanek; Robert H Silverman; Bryan R G Williams
Journal:  Immunology       Date:  2006-08       Impact factor: 7.397

2.  RNA-dependent protein kinase is required for alpha-1 interferon transgene-induced resistance to genital herpes simplex virus type 2.

Authors:  Daniel J J Carr; Lisa Tomanek; Robert H Silverman; Iain L Campbell; Bryan R G Williams
Journal:  J Virol       Date:  2005-07       Impact factor: 5.103

Review 3.  Herpes simplex virus and the chemokines that mediate the inflammation.

Authors:  D J J Carr; L Tomanek
Journal:  Curr Top Microbiol Immunol       Date:  2006       Impact factor: 4.291

4.  Chemokines and Chemokine Receptors Critical to Host Resistance following Genital Herpes Simplex Virus Type 2 (HSV-2) Infection.

Authors:  M Thapa; D J J Carr
Journal:  Open Immunol J       Date:  2008

5.  Local delivery of CpG oligodeoxynucleotides induces rapid changes in the genital mucosa and inhibits replication, but not entry, of herpes simplex virus type 2.

Authors:  Ali A Ashkar; Stefan Bauer; William J Mitchell; Jeff Vieira; Kenneth L Rosenthal
Journal:  J Virol       Date:  2003-08       Impact factor: 5.103

6.  Herpes simplex virus type 2-induced mortality following genital infection is blocked by anti-tumor necrosis factor alpha antibody in CXCL10-deficient mice.

Authors:  Manoj Thapa; Daniel J J Carr
Journal:  J Virol       Date:  2008-08-06       Impact factor: 5.103

7.  Mechanism of reduced T-cell effector functions and class-switched antibody responses to herpes simplex virus type 2 in the absence of B7 costimulation.

Authors:  Lydia G Thebeau; Lynda A Morrison
Journal:  J Virol       Date:  2003-02       Impact factor: 5.103

8.  Interleukin-15 and natural killer and NKT cells play a critical role in innate protection against genital herpes simplex virus type 2 infection.

Authors:  Ali A Ashkar; Kenneth L Rosenthal
Journal:  J Virol       Date:  2003-09       Impact factor: 5.103

9.  Analysis of the cytolytic T-lymphocyte response to herpes simplex virus type 1 glycoprotein B during primary and secondary infection.

Authors:  C T Nugent; R M Wolcott; R Chervenak; S R Jennings
Journal:  J Virol       Date:  1994-11       Impact factor: 5.103

10.  CXCL9 and CXCL10 expression are critical for control of genital herpes simplex virus type 2 infection through mobilization of HSV-specific CTL and NK cells to the nervous system.

Authors:  Manoj Thapa; Robert S Welner; Rosana Pelayo; Daniel J J Carr
Journal:  J Immunol       Date:  2008-01-15       Impact factor: 5.422

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