Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling
Anthrax is an infection caused by pathogenic strains of Bacillus anthracis, which secretes a three-component toxic complex consisting of protective antigen (PA), edema factor (EF), and lethal factor (LF). PA forms binary complexes with either LF or EF and mediates their entry into host cells. Althou...
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| Veröffentlicht in: | The Journal of experimental medicine 2005-02, Vol.201 (3), p.325-331 |
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| container_title | The Journal of experimental medicine |
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| creator | Paccani, Silvia Rossi Tonello, Fiorella Ghittoni, Raffaella Natale, Mariarita Muraro, Lucia D'Elios, Mario Milco Tang, Wei-Jen Montecucco, Cesare Baldari, Cosima T |
| description | Anthrax is an infection caused by pathogenic strains of Bacillus anthracis, which secretes a three-component toxic complex consisting of protective antigen (PA), edema factor (EF), and lethal factor (LF). PA forms binary complexes with either LF or EF and mediates their entry into host cells. Although the initial phases of bacterial growth occur in the lymph node, the host fails to mount an effective immune response. Here, we show that LT and ET are potent suppressors of human T cell activation and proliferation triggered through the antigen receptor. Both LT and ET inhibit the mitogen-activated protein and stress kinase pathways, and both toxins inhibit activation of NFAT and AP-1, two transcription factors essential for cytokine gene expression. These data identify a novel strategy of immune evasion by B. anthracis, based on both effector subunits of the toxic complex, and targeted to a key cellular component of adaptive immunity. |
| doi_str_mv | 10.1084/jem.20041557 |
| format | Article |
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PA forms binary complexes with either LF or EF and mediates their entry into host cells. Although the initial phases of bacterial growth occur in the lymph node, the host fails to mount an effective immune response. Here, we show that LT and ET are potent suppressors of human T cell activation and proliferation triggered through the antigen receptor. Both LT and ET inhibit the mitogen-activated protein and stress kinase pathways, and both toxins inhibit activation of NFAT and AP-1, two transcription factors essential for cytokine gene expression. 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PA forms binary complexes with either LF or EF and mediates their entry into host cells. Although the initial phases of bacterial growth occur in the lymph node, the host fails to mount an effective immune response. Here, we show that LT and ET are potent suppressors of human T cell activation and proliferation triggered through the antigen receptor. Both LT and ET inhibit the mitogen-activated protein and stress kinase pathways, and both toxins inhibit activation of NFAT and AP-1, two transcription factors essential for cytokine gene expression. These data identify a novel strategy of immune evasion by B. anthracis, based on both effector subunits of the toxic complex, and targeted to a key cellular component of adaptive immunity.</description><subject>Anthrax - immunology</subject><subject>Antigens, Bacterial - immunology</subject><subject>Antigens, Bacterial - metabolism</subject><subject>Antigens, CD - immunology</subject><subject>Bacillus anthracis</subject><subject>Bacillus anthracis - metabolism</subject><subject>Bacterial Toxins - immunology</subject><subject>Brief Definitive Report</subject><subject>Cell Line</subject><subject>Humans</subject><subject>Lymphocyte Activation</subject><subject>Receptors, Antigen - metabolism</subject><subject>Signal Transduction - physiology</subject><subject>T-Lymphocytes - immunology</subject><subject>Transcription Factors - genetics</subject><subject>Transcription Factors - metabolism</subject><issn>0022-1007</issn><issn>1540-9538</issn><issn>1892-1007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1P3DAQxa2qqCzQW8-VTz0RGH8l9gUJIaCVkLhQiZvlJLO7RokdbAex_z2p2H6d5vB-em9mHiFfGJwx0PL8CcczDiCZUs0HsmJKQmWU0B_JCoDzigE0h-Qo5ycAJqWqP5FDpmpjoNYr8ngZyja5V1riqw-Z5nmaEuZMH-iwG6dt7HYFqeuKf3HFx0DbHe19TvNUfNhQF4rfYKAJO5xKTDT7TXDDIp2Qg7UbMn7ez2Py8-b64ep7dXd_--Pq8q7qJBOl4sIJ05tat0prCUqA7lsOjVjXjovOtNgylG3TqDWrDfC-0ctR3DGJjUbdi2Ny8e47ze2IfYehJDfYKfnRpZ2Nztv_leC3dhNfLOdMgOCLwbe9QYrPM-ZiR587HAYXMM7ZsiXRGMEW8PQd7FLMOeH6TwgD-6sKu1Rhf1ex4F__XewvvP-9eAMNFobh</recordid><startdate>20050207</startdate><enddate>20050207</enddate><creator>Paccani, Silvia Rossi</creator><creator>Tonello, Fiorella</creator><creator>Ghittoni, Raffaella</creator><creator>Natale, Mariarita</creator><creator>Muraro, Lucia</creator><creator>D'Elios, Mario Milco</creator><creator>Tang, Wei-Jen</creator><creator>Montecucco, Cesare</creator><creator>Baldari, Cosima T</creator><general>The Rockefeller University Press</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QL</scope><scope>7T5</scope><scope>C1K</scope><scope>H94</scope><scope>5PM</scope></search><sort><creationdate>20050207</creationdate><title>Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling</title><author>Paccani, Silvia Rossi ; Tonello, Fiorella ; Ghittoni, Raffaella ; Natale, Mariarita ; Muraro, Lucia ; D'Elios, Mario Milco ; Tang, Wei-Jen ; Montecucco, Cesare ; Baldari, Cosima T</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c413t-23a39d968b588405308db2073f6a23c9beb1e4b775f16902d780222a14e78e8d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Anthrax - immunology</topic><topic>Antigens, Bacterial - immunology</topic><topic>Antigens, Bacterial - metabolism</topic><topic>Antigens, CD - immunology</topic><topic>Bacillus anthracis</topic><topic>Bacillus anthracis - metabolism</topic><topic>Bacterial Toxins - immunology</topic><topic>Brief Definitive Report</topic><topic>Cell Line</topic><topic>Humans</topic><topic>Lymphocyte Activation</topic><topic>Receptors, Antigen - metabolism</topic><topic>Signal Transduction - physiology</topic><topic>T-Lymphocytes - immunology</topic><topic>Transcription Factors - genetics</topic><topic>Transcription Factors - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Paccani, Silvia Rossi</creatorcontrib><creatorcontrib>Tonello, Fiorella</creatorcontrib><creatorcontrib>Ghittoni, Raffaella</creatorcontrib><creatorcontrib>Natale, Mariarita</creatorcontrib><creatorcontrib>Muraro, Lucia</creatorcontrib><creatorcontrib>D'Elios, Mario Milco</creatorcontrib><creatorcontrib>Tang, Wei-Jen</creatorcontrib><creatorcontrib>Montecucco, Cesare</creatorcontrib><creatorcontrib>Baldari, Cosima T</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Immunology Abstracts</collection><collection>Environmental Sciences and Pollution Management</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The Journal of experimental medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Paccani, Silvia Rossi</au><au>Tonello, Fiorella</au><au>Ghittoni, Raffaella</au><au>Natale, Mariarita</au><au>Muraro, Lucia</au><au>D'Elios, Mario Milco</au><au>Tang, Wei-Jen</au><au>Montecucco, Cesare</au><au>Baldari, Cosima T</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling</atitle><jtitle>The Journal of experimental medicine</jtitle><addtitle>J Exp Med</addtitle><date>2005-02-07</date><risdate>2005</risdate><volume>201</volume><issue>3</issue><spage>325</spage><epage>331</epage><pages>325-331</pages><issn>0022-1007</issn><eissn>1540-9538</eissn><eissn>1892-1007</eissn><abstract>Anthrax is an infection caused by pathogenic strains of Bacillus anthracis, which secretes a three-component toxic complex consisting of protective antigen (PA), edema factor (EF), and lethal factor (LF). PA forms binary complexes with either LF or EF and mediates their entry into host cells. Although the initial phases of bacterial growth occur in the lymph node, the host fails to mount an effective immune response. Here, we show that LT and ET are potent suppressors of human T cell activation and proliferation triggered through the antigen receptor. Both LT and ET inhibit the mitogen-activated protein and stress kinase pathways, and both toxins inhibit activation of NFAT and AP-1, two transcription factors essential for cytokine gene expression. These data identify a novel strategy of immune evasion by B. anthracis, based on both effector subunits of the toxic complex, and targeted to a key cellular component of adaptive immunity.</abstract><cop>United States</cop><pub>The Rockefeller University Press</pub><pmid>15699068</pmid><doi>10.1084/jem.20041557</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anthrax - immunology Antigens, Bacterial - immunology Antigens, Bacterial - metabolism Antigens, CD - immunology Bacillus anthracis Bacillus anthracis - metabolism Bacterial Toxins - immunology Brief Definitive Report Cell Line Humans Lymphocyte Activation Receptors, Antigen - metabolism Signal Transduction - physiology T-Lymphocytes - immunology Transcription Factors - genetics Transcription Factors - metabolism |
| title | Anthrax toxins suppress T lymphocyte activation by disrupting antigen receptor signaling |
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