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Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL
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| Zeitschriftentitel: | The Journal of Immunology |
|---|---|
| Personen und Körperschaften: | , , , , , , , , , , , , |
| In: | The Journal of Immunology, 183, 2009, 4, S. 2286-2293 |
| Format: | E-Article |
| Sprache: | Englisch |
| veröffentlicht: |
The American Association of Immunologists
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| Schlagwörter: |
| author_facet |
Pilz, Andreas Kratky, Wolfgang Stockinger, Silvia Simma, Olivia Kalinke, Ulrich Lingnau, Karen von Gabain, Alexander Stoiber, Dagmar Sexl, Veronika Kolbe, Thomas Rülicke, Thomas Müller, Mathias Decker, Thomas Pilz, Andreas Kratky, Wolfgang Stockinger, Silvia Simma, Olivia Kalinke, Ulrich Lingnau, Karen von Gabain, Alexander Stoiber, Dagmar Sexl, Veronika Kolbe, Thomas Rülicke, Thomas Müller, Mathias Decker, Thomas |
|---|---|
| author |
Pilz, Andreas Kratky, Wolfgang Stockinger, Silvia Simma, Olivia Kalinke, Ulrich Lingnau, Karen von Gabain, Alexander Stoiber, Dagmar Sexl, Veronika Kolbe, Thomas Rülicke, Thomas Müller, Mathias Decker, Thomas |
| spellingShingle |
Pilz, Andreas Kratky, Wolfgang Stockinger, Silvia Simma, Olivia Kalinke, Ulrich Lingnau, Karen von Gabain, Alexander Stoiber, Dagmar Sexl, Veronika Kolbe, Thomas Rülicke, Thomas Müller, Mathias Decker, Thomas The Journal of Immunology Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL Immunology Immunology and Allergy |
| author_sort |
pilz, andreas |
| spelling |
Pilz, Andreas Kratky, Wolfgang Stockinger, Silvia Simma, Olivia Kalinke, Ulrich Lingnau, Karen von Gabain, Alexander Stoiber, Dagmar Sexl, Veronika Kolbe, Thomas Rülicke, Thomas Müller, Mathias Decker, Thomas 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.0901383 <jats:title>Abstract</jats:title> <jats:p>Phosphorylation of transcription factor STAT-1 on Y701 regulates subcellular localization whereas phosphorylation of the transactivating domain at S727 enhances transcriptional activity. In this study, we investigate the impact of STAT-1 and the importance of transactivating domain phosphorylation on the induction of peptide-specific CTL in presence of the TLR9-dependent immune adjuvant IC31. STAT-1 deficiency completely abolished CTL induction upon immunization, which was strongly reduced in animals carrying the mutation of the S727 phospho-acceptor site. A comparable reduction of CTL was found in mice lacking the type I IFN (IFN-I) receptor, whereas IFN-γ-deficient mice behaved like wild-type controls. This finding suggests that S727-phosphorylated STAT-1 supports IFN-I-dependent induction of CTL. In adoptive transfer experiments, IFN-I- and S727-phosphorylated STAT-1 were critical for the activation and function of dendritic cells. Mice with a T cell-specific IFN-I receptor ablation did not show impaired CTL responses. Unlike the situation observed for CTL development S727-phosphorylated STAT-1 restrained proliferation of naive CD8+ T cells both in vitro and following transfer into Rag-deficient mice. In summary, our data reveal a dual role of S727-phosphorylated STAT-1 for dendritic cell maturation as a prerequisite for the induction of CTL activity and for T cell autonomous control of activation-induced or homeostatic proliferation.</jats:p> Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL The Journal of Immunology |
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| title |
Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_unstemmed |
Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_full |
Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_fullStr |
Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_full_unstemmed |
Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_short |
Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_sort |
dendritic cells require stat-1 phosphorylated at its transactivating domain for the induction of peptide-specific ctl |
| topic |
Immunology Immunology and Allergy |
| url |
http://dx.doi.org/10.4049/jimmunol.0901383 |
| publishDate |
2009 |
| physical |
2286-2293 |
| description |
<jats:title>Abstract</jats:title>
<jats:p>Phosphorylation of transcription factor STAT-1 on Y701 regulates subcellular localization whereas phosphorylation of the transactivating domain at S727 enhances transcriptional activity. In this study, we investigate the impact of STAT-1 and the importance of transactivating domain phosphorylation on the induction of peptide-specific CTL in presence of the TLR9-dependent immune adjuvant IC31. STAT-1 deficiency completely abolished CTL induction upon immunization, which was strongly reduced in animals carrying the mutation of the S727 phospho-acceptor site. A comparable reduction of CTL was found in mice lacking the type I IFN (IFN-I) receptor, whereas IFN-γ-deficient mice behaved like wild-type controls. This finding suggests that S727-phosphorylated STAT-1 supports IFN-I-dependent induction of CTL. In adoptive transfer experiments, IFN-I- and S727-phosphorylated STAT-1 were critical for the activation and function of dendritic cells. Mice with a T cell-specific IFN-I receptor ablation did not show impaired CTL responses. Unlike the situation observed for CTL development S727-phosphorylated STAT-1 restrained proliferation of naive CD8+ T cells both in vitro and following transfer into Rag-deficient mice. In summary, our data reveal a dual role of S727-phosphorylated STAT-1 for dendritic cell maturation as a prerequisite for the induction of CTL activity and for T cell autonomous control of activation-induced or homeostatic proliferation.</jats:p> |
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| author | Pilz, Andreas, Kratky, Wolfgang, Stockinger, Silvia, Simma, Olivia, Kalinke, Ulrich, Lingnau, Karen, von Gabain, Alexander, Stoiber, Dagmar, Sexl, Veronika, Kolbe, Thomas, Rülicke, Thomas, Müller, Mathias, Decker, Thomas |
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| description | <jats:title>Abstract</jats:title> <jats:p>Phosphorylation of transcription factor STAT-1 on Y701 regulates subcellular localization whereas phosphorylation of the transactivating domain at S727 enhances transcriptional activity. In this study, we investigate the impact of STAT-1 and the importance of transactivating domain phosphorylation on the induction of peptide-specific CTL in presence of the TLR9-dependent immune adjuvant IC31. STAT-1 deficiency completely abolished CTL induction upon immunization, which was strongly reduced in animals carrying the mutation of the S727 phospho-acceptor site. A comparable reduction of CTL was found in mice lacking the type I IFN (IFN-I) receptor, whereas IFN-γ-deficient mice behaved like wild-type controls. This finding suggests that S727-phosphorylated STAT-1 supports IFN-I-dependent induction of CTL. In adoptive transfer experiments, IFN-I- and S727-phosphorylated STAT-1 were critical for the activation and function of dendritic cells. Mice with a T cell-specific IFN-I receptor ablation did not show impaired CTL responses. Unlike the situation observed for CTL development S727-phosphorylated STAT-1 restrained proliferation of naive CD8+ T cells both in vitro and following transfer into Rag-deficient mice. In summary, our data reveal a dual role of S727-phosphorylated STAT-1 for dendritic cell maturation as a prerequisite for the induction of CTL activity and for T cell autonomous control of activation-induced or homeostatic proliferation.</jats:p> |
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| institution | DE-Gla1, DE-Zi4, DE-15, DE-Rs1, DE-Pl11, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-Zwi2, DE-D161 |
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| spelling | Pilz, Andreas Kratky, Wolfgang Stockinger, Silvia Simma, Olivia Kalinke, Ulrich Lingnau, Karen von Gabain, Alexander Stoiber, Dagmar Sexl, Veronika Kolbe, Thomas Rülicke, Thomas Müller, Mathias Decker, Thomas 0022-1767 1550-6606 The American Association of Immunologists Immunology Immunology and Allergy http://dx.doi.org/10.4049/jimmunol.0901383 <jats:title>Abstract</jats:title> <jats:p>Phosphorylation of transcription factor STAT-1 on Y701 regulates subcellular localization whereas phosphorylation of the transactivating domain at S727 enhances transcriptional activity. In this study, we investigate the impact of STAT-1 and the importance of transactivating domain phosphorylation on the induction of peptide-specific CTL in presence of the TLR9-dependent immune adjuvant IC31. STAT-1 deficiency completely abolished CTL induction upon immunization, which was strongly reduced in animals carrying the mutation of the S727 phospho-acceptor site. A comparable reduction of CTL was found in mice lacking the type I IFN (IFN-I) receptor, whereas IFN-γ-deficient mice behaved like wild-type controls. This finding suggests that S727-phosphorylated STAT-1 supports IFN-I-dependent induction of CTL. In adoptive transfer experiments, IFN-I- and S727-phosphorylated STAT-1 were critical for the activation and function of dendritic cells. Mice with a T cell-specific IFN-I receptor ablation did not show impaired CTL responses. Unlike the situation observed for CTL development S727-phosphorylated STAT-1 restrained proliferation of naive CD8+ T cells both in vitro and following transfer into Rag-deficient mice. In summary, our data reveal a dual role of S727-phosphorylated STAT-1 for dendritic cell maturation as a prerequisite for the induction of CTL activity and for T cell autonomous control of activation-induced or homeostatic proliferation.</jats:p> Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL The Journal of Immunology |
| spellingShingle | Pilz, Andreas, Kratky, Wolfgang, Stockinger, Silvia, Simma, Olivia, Kalinke, Ulrich, Lingnau, Karen, von Gabain, Alexander, Stoiber, Dagmar, Sexl, Veronika, Kolbe, Thomas, Rülicke, Thomas, Müller, Mathias, Decker, Thomas, The Journal of Immunology, Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL, Immunology, Immunology and Allergy |
| title | Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_full | Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_fullStr | Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_full_unstemmed | Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_short | Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| title_sort | dendritic cells require stat-1 phosphorylated at its transactivating domain for the induction of peptide-specific ctl |
| title_unstemmed | Dendritic Cells Require STAT-1 Phosphorylated at Its Transactivating Domain for the Induction of Peptide-Specific CTL |
| topic | Immunology, Immunology and Allergy |
| url | http://dx.doi.org/10.4049/jimmunol.0901383 |