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Protective immunity to genital herpes simplex [correction of simpex] virus type 2 infection is mediated by T-bet.

Artikel i vetenskaplig tidskrift
Författare Alexandra Svensson
Inger Nordström
Jia-Bin Sun
Kristina Eriksson
Publicerad i Journal of immunology (Baltimore, Md. : 1950)
Volym 174
Nummer/häfte 10
Sidor 6266-73
ISSN 0022-1767
Publiceringsår 2005
Publicerad vid Institutionen för invärtesmedicin, Avdelningen för reumatologi och inflammationsforskning
Institutionen för medicinsk mikrobiologi och immunologi
Sidor 6266-73
Språk en
Länkar www.ncbi.nlm.nih.gov/entrez/query.f...
Ämnesord Animals, Antibodies, Viral, biosynthesis, CD4-Positive T-Lymphocytes, immunology, metabolism, virology, CD8-Positive T-Lymphocytes, immunology, metabolism, virology, CHO Cells, Cricetinae, Cytotoxicity Tests, Immunologic, Epitopes, T-Lymphocyte, immunology, Female, Herpes Genitalis, genetics, immunology, mortality, Herpes Simplex Virus Vaccines, administration & dosage, immunology, Herpesvirus 2, Human, immunology, Immunity, Active, genetics, Immunity, Natural, genetics, Immunologic Deficiency Syndromes, genetics, immunology, mortality, Killer Cells, Natural, immunology, virology, Mice, Mice, Inbred C57BL, T-Box Domain Proteins, Transcription Factors, deficiency, genetics, physiology, Virus Replication, genetics, immunology
Ämneskategorier Mikrobiologi inom det medicinska området

Sammanfattning

We show, for the first time, that the transcription factor T-bet, which is implicated in IFN-gamma production, is required for the induction of vaccine-induced antiviral immune protection. T-bet was found to be important in both the innate and acquired immune protection against genital HSV-2 infection. T-bet(-/-) and T-bet(+/+) mice were infected vaginally with HSV-2 and examined daily for disease and mortality. T-bet(-/-) mice had significantly higher virus titers than T-bet(+/+) mice following a primary HSV-2 infection, and succumbed significantly earlier to the infection. This result was associated with an impaired NK cell cytotoxic capacity and NK cell-mediated IFN-gamma production in the T-bet(-/-) mice. To assess the induction of acquired antiviral immune protection, mice were vaccinated with an attenuated virus before infection. Vaccinated T-bet(-/-) mice could not control viral replication following an HSV-2 challenge and had significantly higher virus titers and mortality rates than vaccinated T-bet(+/+) mice that remained healthy. The impaired acquired immune protection in T-bet(-/-) mice was associated with a significantly decreased HSV-2-specific delayed-type hypersensitivity response and a significantly reduced HSV-2-specific IFN-gamma production from CD4(+) T cells. However, T-bet deficiency did not impair either the IFN-gamma production or the cytotoxic capacity of HSV-2-specific CD8(+) T cells. We conclude that T-bet plays a crucial role in both the innate defense and the generation of vaccine-induced immunity against genital HSV-2 infection in mice.

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