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T-cell STAT3 is required for the maintenance of humoral immunity to LCMV.

McIlwain DR, Grusdat M, Pozdeev VI, Xu HC, Shinde P, Reardon C, Hao Z, Beyer M, Bergthaler A, Häussinger D, Nolan GP, Lang KS, Lang PA - Eur. J. Immunol. (2014)

Bottom Line: STAT3 is a critical transcription factor activated downstream of cytokine signaling and is integral for the function of multiple immune cell types.As a result, STAT3 T cell deficient mice produced attenuated germinal center reactions, and did not accumulate bone marrow virus specific IgG-secreting cells, resulting in failure to maintain levels of virus-specific IgG or mount neutralizing responses to LCMV in the serum.These effects were associated with reduced control of viral replication and prolonged infection.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany; Baxter Laboratory in Stem Cell Biology, Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.

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Reduced longevity of chronically infected STAT3 T-cell-deficient mice. Lck-Cre−Stat3fl/fl vs. Lck-Cre+Stat3fl/fl mice were infected with 2 × 103 PFU LCMV-Docile. Survival of infected mice was monitored over time (n = 7–8 mice/group). Data shown are pooled from two independent experiments. Statistical significance was determined by Kaplan–Meier log rank test.
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fig05: Reduced longevity of chronically infected STAT3 T-cell-deficient mice. Lck-Cre−Stat3fl/fl vs. Lck-Cre+Stat3fl/fl mice were infected with 2 × 103 PFU LCMV-Docile. Survival of infected mice was monitored over time (n = 7–8 mice/group). Data shown are pooled from two independent experiments. Statistical significance was determined by Kaplan–Meier log rank test.

Mentions: Prolonged infections of noncytolytic viruses can lead to toxic immunopathology [29–31]. When we tested long-term survival following LCMV infection we found that STAT3 deficiency was associated with significantly earlier demise (Fig.5). Thus impaired Tfh function, reduced humoral immunity, and diminished control of viral replication appears to reduce long-term survival of Lck-Cre+Stat3fl/fl vs. Lck-Cre−Stat3fl/fl mice following chronic LCMV infection.


T-cell STAT3 is required for the maintenance of humoral immunity to LCMV.

McIlwain DR, Grusdat M, Pozdeev VI, Xu HC, Shinde P, Reardon C, Hao Z, Beyer M, Bergthaler A, Häussinger D, Nolan GP, Lang KS, Lang PA - Eur. J. Immunol. (2014)

Reduced longevity of chronically infected STAT3 T-cell-deficient mice. Lck-Cre−Stat3fl/fl vs. Lck-Cre+Stat3fl/fl mice were infected with 2 × 103 PFU LCMV-Docile. Survival of infected mice was monitored over time (n = 7–8 mice/group). Data shown are pooled from two independent experiments. Statistical significance was determined by Kaplan–Meier log rank test.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4383653&req=5

fig05: Reduced longevity of chronically infected STAT3 T-cell-deficient mice. Lck-Cre−Stat3fl/fl vs. Lck-Cre+Stat3fl/fl mice were infected with 2 × 103 PFU LCMV-Docile. Survival of infected mice was monitored over time (n = 7–8 mice/group). Data shown are pooled from two independent experiments. Statistical significance was determined by Kaplan–Meier log rank test.
Mentions: Prolonged infections of noncytolytic viruses can lead to toxic immunopathology [29–31]. When we tested long-term survival following LCMV infection we found that STAT3 deficiency was associated with significantly earlier demise (Fig.5). Thus impaired Tfh function, reduced humoral immunity, and diminished control of viral replication appears to reduce long-term survival of Lck-Cre+Stat3fl/fl vs. Lck-Cre−Stat3fl/fl mice following chronic LCMV infection.

Bottom Line: STAT3 is a critical transcription factor activated downstream of cytokine signaling and is integral for the function of multiple immune cell types.As a result, STAT3 T cell deficient mice produced attenuated germinal center reactions, and did not accumulate bone marrow virus specific IgG-secreting cells, resulting in failure to maintain levels of virus-specific IgG or mount neutralizing responses to LCMV in the serum.These effects were associated with reduced control of viral replication and prolonged infection.

View Article: PubMed Central - PubMed

Affiliation: Department of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Düsseldorf, Germany; Baxter Laboratory in Stem Cell Biology, Department of Microbiology and Immunology, Stanford University, Stanford, CA, USA.

Show MeSH
Related in: MedlinePlus