Aurora A controls CD8+ T cell cytotoxic activity and antiviral response
Aurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4 + T cell activation and, also, in graft versus host disease development. However, it remains unknown wheth...
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| description | Aurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4
+
T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8
+
T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8
+
T cells. This finding was similarly proven for both mice and human CD8
+
CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as
granzyme B
or
perforin1
. Finally, we have found that Aurora A is necessary for CD8
+
T cell-mediated antiviral response, in an
in vivo
model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats. |
| doi_str_mv | 10.1038/s41598-019-38647-y |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_6379542</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2183739966</sourcerecordid><originalsourceid>FETCH-LOGICAL-c474t-6ce683735755b3cb3ab67ecf5ca8be08a712bbd871d0a71d69803084eadebe4b3</originalsourceid><addsrcrecordid>eNp9kU1LAzEQhoMoKto_4EECXgRZzXeyF6HUTxC86Dkk2VRXtpua7Bb335tarR8HAyET5pl3ZngBOMDoFCOqzhLDvFQFwmVBlWCyGDbALkGMF4QSsvkj3gGjlF5QPpyUDJfbYIciKRXGdBdcj_sYooFj6ELbxdAkOLlQJ_ABOt800A1d6MJb7aBxXb2ouwGatsp3-YmmgdGneWiT3wdbU9MkP_p898Dj1eXD5Ka4u7--nYzvCsck6wrhvFBUUi45t9RZaqyQ3k25M8p6pIzExNpKSVyhHFeiVIgixbypvPXM0j1wvtKd93bmK-fz0KbR81jPTBx0MLX-nWnrZ_0UFlpQWXJGssDxp0AMr71PnZ7VabmraX3okyZYUcGRFCijR3_Ql9DHNq_3QUlalkJkiqwoF0NK0U_Xw2Ckl1bplVU6W6U_rNJDLjr8uca65MuYDNAVkHKqffLxu_c_su9bWZ_f</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2183739966</pqid></control><display><type>article</type><title>Aurora A controls CD8+ T cell cytotoxic activity and antiviral response</title><source>Nature Open Access</source><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central</source><source>Springer Nature OA/Free Journals</source><source>Free Full-Text Journals in Chemistry</source><creator>Bustos-Morán, Eugenio ; Blas-Rus, Noelia ; Alcaraz-Serna, Ana ; Iborra, Salvador ; González-Martínez, José ; Malumbres, Marcos ; Sánchez-Madrid, Francisco</creator><creatorcontrib>Bustos-Morán, Eugenio ; Blas-Rus, Noelia ; Alcaraz-Serna, Ana ; Iborra, Salvador ; González-Martínez, José ; Malumbres, Marcos ; Sánchez-Madrid, Francisco</creatorcontrib><description>Aurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4
+
T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8
+
T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8
+
T cells. This finding was similarly proven for both mice and human CD8
+
CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as
granzyme B
or
perforin1
. Finally, we have found that Aurora A is necessary for CD8
+
T cell-mediated antiviral response, in an
in vivo
model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-38647-y</identifier><identifier>PMID: 30778113</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>38 ; 38/77 ; 631/250/1619/554 ; 631/250/2152 ; 82 ; 96 ; 96/1 ; 96/31 ; 96/95 ; Animals ; Antiviral drugs ; Aurora Kinase A - antagonists & inhibitors ; Aurora Kinase A - genetics ; CD4 antigen ; CD8 antigen ; CD8-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - metabolism ; Cell activation ; Cell cycle ; Cytotoxicity ; Cytotoxicity, Immunologic - genetics ; Degranulation ; Disease Models, Animal ; Graft-versus-host reaction ; Granzyme B ; Host-Pathogen Interactions - genetics ; Host-Pathogen Interactions - immunology ; Humanities and Social Sciences ; Humans ; Immunomodulation - genetics ; Lymphocyte Activation - genetics ; Lymphocyte Activation - immunology ; Lymphocytes ; Lymphocytes B ; Lymphocytes T ; Male ; Mice ; Mice, Transgenic ; multidisciplinary ; Perforin ; Protein-serine/threonine kinase ; Receptors, Antigen, T-Cell - metabolism ; Science ; Science (multidisciplinary) ; Signal Transduction ; Transcription activation ; Tumors ; Vaccinia - genetics ; Vaccinia - immunology ; Vaccinia - virology ; Vaccinia virus - immunology ; Virus Diseases - genetics ; Virus Diseases - immunology ; Virus Diseases - virology</subject><ispartof>Scientific reports, 2019-02, Vol.9 (1), p.2211-2211, Article 2211</ispartof><rights>The Author(s) 2019</rights><rights>This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-6ce683735755b3cb3ab67ecf5ca8be08a712bbd871d0a71d69803084eadebe4b3</citedby><cites>FETCH-LOGICAL-c474t-6ce683735755b3cb3ab67ecf5ca8be08a712bbd871d0a71d69803084eadebe4b3</cites><orcidid>0000-0002-0829-6315</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379542/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6379542/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27923,27924,41119,42188,51575,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30778113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bustos-Morán, Eugenio</creatorcontrib><creatorcontrib>Blas-Rus, Noelia</creatorcontrib><creatorcontrib>Alcaraz-Serna, Ana</creatorcontrib><creatorcontrib>Iborra, Salvador</creatorcontrib><creatorcontrib>González-Martínez, José</creatorcontrib><creatorcontrib>Malumbres, Marcos</creatorcontrib><creatorcontrib>Sánchez-Madrid, Francisco</creatorcontrib><title>Aurora A controls CD8+ T cell cytotoxic activity and antiviral response</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Aurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4
+
T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8
+
T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8
+
T cells. This finding was similarly proven for both mice and human CD8
+
CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as
granzyme B
or
perforin1
. Finally, we have found that Aurora A is necessary for CD8
+
T cell-mediated antiviral response, in an
in vivo
model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats.</description><subject>38</subject><subject>38/77</subject><subject>631/250/1619/554</subject><subject>631/250/2152</subject><subject>82</subject><subject>96</subject><subject>96/1</subject><subject>96/31</subject><subject>96/95</subject><subject>Animals</subject><subject>Antiviral drugs</subject><subject>Aurora Kinase A - antagonists & inhibitors</subject><subject>Aurora Kinase A - genetics</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>Cell activation</subject><subject>Cell cycle</subject><subject>Cytotoxicity</subject><subject>Cytotoxicity, Immunologic - genetics</subject><subject>Degranulation</subject><subject>Disease Models, Animal</subject><subject>Graft-versus-host reaction</subject><subject>Granzyme B</subject><subject>Host-Pathogen Interactions - genetics</subject><subject>Host-Pathogen Interactions - immunology</subject><subject>Humanities and Social Sciences</subject><subject>Humans</subject><subject>Immunomodulation - genetics</subject><subject>Lymphocyte Activation - genetics</subject><subject>Lymphocyte Activation - immunology</subject><subject>Lymphocytes</subject><subject>Lymphocytes B</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>multidisciplinary</subject><subject>Perforin</subject><subject>Protein-serine/threonine kinase</subject><subject>Receptors, Antigen, T-Cell - metabolism</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Signal Transduction</subject><subject>Transcription activation</subject><subject>Tumors</subject><subject>Vaccinia - genetics</subject><subject>Vaccinia - immunology</subject><subject>Vaccinia - virology</subject><subject>Vaccinia virus - immunology</subject><subject>Virus Diseases - 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antagonists & inhibitors</topic><topic>Aurora Kinase A - genetics</topic><topic>CD4 antigen</topic><topic>CD8 antigen</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - metabolism</topic><topic>Cell activation</topic><topic>Cell cycle</topic><topic>Cytotoxicity</topic><topic>Cytotoxicity, Immunologic - genetics</topic><topic>Degranulation</topic><topic>Disease Models, Animal</topic><topic>Graft-versus-host reaction</topic><topic>Granzyme B</topic><topic>Host-Pathogen Interactions - genetics</topic><topic>Host-Pathogen Interactions - immunology</topic><topic>Humanities and Social Sciences</topic><topic>Humans</topic><topic>Immunomodulation - genetics</topic><topic>Lymphocyte Activation - genetics</topic><topic>Lymphocyte Activation - immunology</topic><topic>Lymphocytes</topic><topic>Lymphocytes B</topic><topic>Lymphocytes T</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>multidisciplinary</topic><topic>Perforin</topic><topic>Protein-serine/threonine kinase</topic><topic>Receptors, Antigen, T-Cell - metabolism</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Signal Transduction</topic><topic>Transcription activation</topic><topic>Tumors</topic><topic>Vaccinia - genetics</topic><topic>Vaccinia - immunology</topic><topic>Vaccinia - virology</topic><topic>Vaccinia virus - immunology</topic><topic>Virus Diseases - genetics</topic><topic>Virus Diseases - immunology</topic><topic>Virus Diseases - virology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bustos-Morán, Eugenio</creatorcontrib><creatorcontrib>Blas-Rus, Noelia</creatorcontrib><creatorcontrib>Alcaraz-Serna, Ana</creatorcontrib><creatorcontrib>Iborra, Salvador</creatorcontrib><creatorcontrib>González-Martínez, José</creatorcontrib><creatorcontrib>Malumbres, Marcos</creatorcontrib><creatorcontrib>Sánchez-Madrid, Francisco</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bustos-Morán, Eugenio</au><au>Blas-Rus, Noelia</au><au>Alcaraz-Serna, Ana</au><au>Iborra, Salvador</au><au>González-Martínez, José</au><au>Malumbres, Marcos</au><au>Sánchez-Madrid, Francisco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Aurora A controls CD8+ T cell cytotoxic activity and antiviral response</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-02-18</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>2211</spage><epage>2211</epage><pages>2211-2211</pages><artnum>2211</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Aurora A is a serine/threonine kinase whose role in cell cycle progression and tumour generation has been widely studied. Recent work has revealed an unexpected function for Aurora A during CD4
+
T cell activation and, also, in graft versus host disease development. However, it remains unknown whether Aurora A is involved in CD8
+
T cell effector function and in cytotoxic T lymphocyte-mediated antiviral response. Here, we show that Aurora A chemical inhibition leads to an impairment of both the peptide-specific cytotoxicity and the degranulation activity of CD8
+
T cells. This finding was similarly proven for both mice and human CD8
+
CTL activity. As a result of Aurora A blockade, we detected a reduction in the expression induced by T cell activation of genes classically related to the effector function of cytotoxic T lymphocytes such as
granzyme B
or
perforin1
. Finally, we have found that Aurora A is necessary for CD8
+
T cell-mediated antiviral response, in an
in vivo
model of vaccinia virus infection. Thus, we can conclude that Aurora A activity is, indeed, needed for the proper effector function of cytotoxic T lymphocytes and for their activity against viral threats.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>30778113</pmid><doi>10.1038/s41598-019-38647-y</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-0829-6315</orcidid><oa>free_for_read</oa></addata></record> |
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| source | Nature Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Springer Nature OA/Free Journals; Free Full-Text Journals in Chemistry |
| subjects | 38 38/77 631/250/1619/554 631/250/2152 82 96 96/1 96/31 96/95 Animals Antiviral drugs Aurora Kinase A - antagonists & inhibitors Aurora Kinase A - genetics CD4 antigen CD8 antigen CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - metabolism Cell activation Cell cycle Cytotoxicity Cytotoxicity, Immunologic - genetics Degranulation Disease Models, Animal Graft-versus-host reaction Granzyme B Host-Pathogen Interactions - genetics Host-Pathogen Interactions - immunology Humanities and Social Sciences Humans Immunomodulation - genetics Lymphocyte Activation - genetics Lymphocyte Activation - immunology Lymphocytes Lymphocytes B Lymphocytes T Male Mice Mice, Transgenic multidisciplinary Perforin Protein-serine/threonine kinase Receptors, Antigen, T-Cell - metabolism Science Science (multidisciplinary) Signal Transduction Transcription activation Tumors Vaccinia - genetics Vaccinia - immunology Vaccinia - virology Vaccinia virus - immunology Virus Diseases - genetics Virus Diseases - immunology Virus Diseases - virology |
| title | Aurora A controls CD8+ T cell cytotoxic activity and antiviral response |
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