author_facet Bardet, Maureen
Unterreiner, Adeline
Malinverni, Claire
Lafossas, Frédérique
Vedrine, Corinne
Boesch, Danielle
Kolb, Yeter
Kaiser, Daniel
Glück, Anton
Schneider, Martin A
Katopodis, Andreas
Renatus, Martin
Simic, Oliver
Schlapbach, Achim
Quancard, Jean
Régnier, Catherine H
Bold, Guido
Pissot‐Soldermann, Carole
Carballido, José M
Kovarik, Jiri
Calzascia, Thomas
Bornancin, Frédéric
Bardet, Maureen
Unterreiner, Adeline
Malinverni, Claire
Lafossas, Frédérique
Vedrine, Corinne
Boesch, Danielle
Kolb, Yeter
Kaiser, Daniel
Glück, Anton
Schneider, Martin A
Katopodis, Andreas
Renatus, Martin
Simic, Oliver
Schlapbach, Achim
Quancard, Jean
Régnier, Catherine H
Bold, Guido
Pissot‐Soldermann, Carole
Carballido, José M
Kovarik, Jiri
Calzascia, Thomas
Bornancin, Frédéric
author Bardet, Maureen
Unterreiner, Adeline
Malinverni, Claire
Lafossas, Frédérique
Vedrine, Corinne
Boesch, Danielle
Kolb, Yeter
Kaiser, Daniel
Glück, Anton
Schneider, Martin A
Katopodis, Andreas
Renatus, Martin
Simic, Oliver
Schlapbach, Achim
Quancard, Jean
Régnier, Catherine H
Bold, Guido
Pissot‐Soldermann, Carole
Carballido, José M
Kovarik, Jiri
Calzascia, Thomas
Bornancin, Frédéric
spellingShingle Bardet, Maureen
Unterreiner, Adeline
Malinverni, Claire
Lafossas, Frédérique
Vedrine, Corinne
Boesch, Danielle
Kolb, Yeter
Kaiser, Daniel
Glück, Anton
Schneider, Martin A
Katopodis, Andreas
Renatus, Martin
Simic, Oliver
Schlapbach, Achim
Quancard, Jean
Régnier, Catherine H
Bold, Guido
Pissot‐Soldermann, Carole
Carballido, José M
Kovarik, Jiri
Calzascia, Thomas
Bornancin, Frédéric
Immunology & Cell Biology
The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
Cell Biology
Immunology
Immunology and Allergy
author_sort bardet, maureen
spelling Bardet, Maureen Unterreiner, Adeline Malinverni, Claire Lafossas, Frédérique Vedrine, Corinne Boesch, Danielle Kolb, Yeter Kaiser, Daniel Glück, Anton Schneider, Martin A Katopodis, Andreas Renatus, Martin Simic, Oliver Schlapbach, Achim Quancard, Jean Régnier, Catherine H Bold, Guido Pissot‐Soldermann, Carole Carballido, José M Kovarik, Jiri Calzascia, Thomas Bornancin, Frédéric 0818-9641 1440-1711 Wiley Cell Biology Immunology Immunology and Allergy http://dx.doi.org/10.1111/imcb.1018 <jats:title>Abstract</jats:title><jats:p>Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is essential for immune responses triggered by antigen receptors but the contribution of its paracaspase activity is not fully understood. Here, we studied how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 proteolytic function regulates T‐cell activation and fate after engagement of the T‐cell receptor pathway. We show that <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827, a potent and selective <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase inhibitor, does not prevent the initial phase of T‐cell activation, in contrast to the pan‐protein kinase C inhibitor <jats:styled-content style="fixed-case">AEB</jats:styled-content>071. However, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 strongly impacted cell expansion after activation. We demonstrate this is the consequence of profound inhibition of <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 production as well as reduced expression of the <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 receptor alpha subunit (<jats:styled-content style="fixed-case">CD</jats:styled-content>25), resulting from defective canonical <jats:styled-content style="fixed-case">NF</jats:styled-content>‐κB activation and accelerated <jats:styled-content style="fixed-case">mRNA</jats:styled-content> turnover mechanisms. Accordingly, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 revealed a unique transcriptional fingerprint of <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 protease activity, providing evidence for broad control of T‐cell signaling pathways. Altogether, this first report with a potent and selective inhibitor elucidates how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase activity integrates several T‐cell activation pathways and indirectly controls gamma‐chain receptor dependent survival, to impact on T‐cell expansion.</jats:p> The T‐cell fingerprint of <scp>MALT</scp>1 paracaspase revealed by selective inhibition Immunology & Cell Biology
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title The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_unstemmed The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_full The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_fullStr The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_full_unstemmed The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_short The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_sort the t‐cell fingerprint of <scp>malt</scp>1 paracaspase revealed by selective inhibition
topic Cell Biology
Immunology
Immunology and Allergy
url http://dx.doi.org/10.1111/imcb.1018
publishDate 2018
physical 81-99
description <jats:title>Abstract</jats:title><jats:p>Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is essential for immune responses triggered by antigen receptors but the contribution of its paracaspase activity is not fully understood. Here, we studied how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 proteolytic function regulates T‐cell activation and fate after engagement of the T‐cell receptor pathway. We show that <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827, a potent and selective <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase inhibitor, does not prevent the initial phase of T‐cell activation, in contrast to the pan‐protein kinase C inhibitor <jats:styled-content style="fixed-case">AEB</jats:styled-content>071. However, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 strongly impacted cell expansion after activation. We demonstrate this is the consequence of profound inhibition of <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 production as well as reduced expression of the <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 receptor alpha subunit (<jats:styled-content style="fixed-case">CD</jats:styled-content>25), resulting from defective canonical <jats:styled-content style="fixed-case">NF</jats:styled-content>‐κB activation and accelerated <jats:styled-content style="fixed-case">mRNA</jats:styled-content> turnover mechanisms. Accordingly, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 revealed a unique transcriptional fingerprint of <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 protease activity, providing evidence for broad control of T‐cell signaling pathways. Altogether, this first report with a potent and selective inhibitor elucidates how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase activity integrates several T‐cell activation pathways and indirectly controls gamma‐chain receptor dependent survival, to impact on T‐cell expansion.</jats:p>
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author Bardet, Maureen, Unterreiner, Adeline, Malinverni, Claire, Lafossas, Frédérique, Vedrine, Corinne, Boesch, Danielle, Kolb, Yeter, Kaiser, Daniel, Glück, Anton, Schneider, Martin A, Katopodis, Andreas, Renatus, Martin, Simic, Oliver, Schlapbach, Achim, Quancard, Jean, Régnier, Catherine H, Bold, Guido, Pissot‐Soldermann, Carole, Carballido, José M, Kovarik, Jiri, Calzascia, Thomas, Bornancin, Frédéric
author_facet Bardet, Maureen, Unterreiner, Adeline, Malinverni, Claire, Lafossas, Frédérique, Vedrine, Corinne, Boesch, Danielle, Kolb, Yeter, Kaiser, Daniel, Glück, Anton, Schneider, Martin A, Katopodis, Andreas, Renatus, Martin, Simic, Oliver, Schlapbach, Achim, Quancard, Jean, Régnier, Catherine H, Bold, Guido, Pissot‐Soldermann, Carole, Carballido, José M, Kovarik, Jiri, Calzascia, Thomas, Bornancin, Frédéric, Bardet, Maureen, Unterreiner, Adeline, Malinverni, Claire, Lafossas, Frédérique, Vedrine, Corinne, Boesch, Danielle, Kolb, Yeter, Kaiser, Daniel, Glück, Anton, Schneider, Martin A, Katopodis, Andreas, Renatus, Martin, Simic, Oliver, Schlapbach, Achim, Quancard, Jean, Régnier, Catherine H, Bold, Guido, Pissot‐Soldermann, Carole, Carballido, José M, Kovarik, Jiri, Calzascia, Thomas, Bornancin, Frédéric
author_sort bardet, maureen
container_issue 1
container_start_page 81
container_title Immunology & Cell Biology
container_volume 96
description <jats:title>Abstract</jats:title><jats:p>Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is essential for immune responses triggered by antigen receptors but the contribution of its paracaspase activity is not fully understood. Here, we studied how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 proteolytic function regulates T‐cell activation and fate after engagement of the T‐cell receptor pathway. We show that <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827, a potent and selective <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase inhibitor, does not prevent the initial phase of T‐cell activation, in contrast to the pan‐protein kinase C inhibitor <jats:styled-content style="fixed-case">AEB</jats:styled-content>071. However, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 strongly impacted cell expansion after activation. We demonstrate this is the consequence of profound inhibition of <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 production as well as reduced expression of the <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 receptor alpha subunit (<jats:styled-content style="fixed-case">CD</jats:styled-content>25), resulting from defective canonical <jats:styled-content style="fixed-case">NF</jats:styled-content>‐κB activation and accelerated <jats:styled-content style="fixed-case">mRNA</jats:styled-content> turnover mechanisms. Accordingly, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 revealed a unique transcriptional fingerprint of <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 protease activity, providing evidence for broad control of T‐cell signaling pathways. Altogether, this first report with a potent and selective inhibitor elucidates how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase activity integrates several T‐cell activation pathways and indirectly controls gamma‐chain receptor dependent survival, to impact on T‐cell expansion.</jats:p>
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institution DE-Pl11, DE-Rs1, DE-105, DE-14, DE-Ch1, DE-L229, DE-D275, DE-Bn3, DE-Brt1, DE-D161, DE-Gla1, DE-Zi4, DE-15
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spelling Bardet, Maureen Unterreiner, Adeline Malinverni, Claire Lafossas, Frédérique Vedrine, Corinne Boesch, Danielle Kolb, Yeter Kaiser, Daniel Glück, Anton Schneider, Martin A Katopodis, Andreas Renatus, Martin Simic, Oliver Schlapbach, Achim Quancard, Jean Régnier, Catherine H Bold, Guido Pissot‐Soldermann, Carole Carballido, José M Kovarik, Jiri Calzascia, Thomas Bornancin, Frédéric 0818-9641 1440-1711 Wiley Cell Biology Immunology Immunology and Allergy http://dx.doi.org/10.1111/imcb.1018 <jats:title>Abstract</jats:title><jats:p>Mucosa‐associated lymphoid tissue lymphoma translocation protein 1 (MALT1) is essential for immune responses triggered by antigen receptors but the contribution of its paracaspase activity is not fully understood. Here, we studied how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 proteolytic function regulates T‐cell activation and fate after engagement of the T‐cell receptor pathway. We show that <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827, a potent and selective <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase inhibitor, does not prevent the initial phase of T‐cell activation, in contrast to the pan‐protein kinase C inhibitor <jats:styled-content style="fixed-case">AEB</jats:styled-content>071. However, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 strongly impacted cell expansion after activation. We demonstrate this is the consequence of profound inhibition of <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 production as well as reduced expression of the <jats:styled-content style="fixed-case">IL</jats:styled-content>‐2 receptor alpha subunit (<jats:styled-content style="fixed-case">CD</jats:styled-content>25), resulting from defective canonical <jats:styled-content style="fixed-case">NF</jats:styled-content>‐κB activation and accelerated <jats:styled-content style="fixed-case">mRNA</jats:styled-content> turnover mechanisms. Accordingly, <jats:styled-content style="fixed-case">MLT</jats:styled-content>‐827 revealed a unique transcriptional fingerprint of <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 protease activity, providing evidence for broad control of T‐cell signaling pathways. Altogether, this first report with a potent and selective inhibitor elucidates how <jats:styled-content style="fixed-case">MALT</jats:styled-content>1 paracaspase activity integrates several T‐cell activation pathways and indirectly controls gamma‐chain receptor dependent survival, to impact on T‐cell expansion.</jats:p> The T‐cell fingerprint of <scp>MALT</scp>1 paracaspase revealed by selective inhibition Immunology & Cell Biology
spellingShingle Bardet, Maureen, Unterreiner, Adeline, Malinverni, Claire, Lafossas, Frédérique, Vedrine, Corinne, Boesch, Danielle, Kolb, Yeter, Kaiser, Daniel, Glück, Anton, Schneider, Martin A, Katopodis, Andreas, Renatus, Martin, Simic, Oliver, Schlapbach, Achim, Quancard, Jean, Régnier, Catherine H, Bold, Guido, Pissot‐Soldermann, Carole, Carballido, José M, Kovarik, Jiri, Calzascia, Thomas, Bornancin, Frédéric, Immunology & Cell Biology, The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition, Cell Biology, Immunology, Immunology and Allergy
title The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_full The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_fullStr The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_full_unstemmed The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_short The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
title_sort the t‐cell fingerprint of <scp>malt</scp>1 paracaspase revealed by selective inhibition
title_unstemmed The T‐cell fingerprint of MALT1 paracaspase revealed by selective inhibition
topic Cell Biology, Immunology, Immunology and Allergy
url http://dx.doi.org/10.1111/imcb.1018