BCL6b Mediates the Enhanced Magnitude of the Secondary Response of Memory CD8+ T Lymphocytes
A characteristic of the secondary response of CD8+ T cells that distinguishes it from the primary response is the generation of greater numbers of effector cells. Because effector CD8+ T cells are derived from a pool of less differentiated, replicating cells in secondary lymphoid organs, and because...
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| Veröffentlicht in: | Proceedings of the National Academy of Sciences - PNAS 2005-05, Vol.102 (21), p.7418-7425 |
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| creator | Manders, Peter M. Hunter, Patricia J. Telaranta, Aino I. Carr, James M. Marshall, Jennifer L. Carrasco, Marlene Murakami, Yusuke Palmowski, Michael J. Cerundolo, Vincenzo Kaech, Susan M. Ahmed, Rafi Fearon, Douglas T. |
| description | A characteristic of the secondary response of CD8+ T cells that distinguishes it from the primary response is the generation of greater numbers of effector cells. Because effector CD8+ T cells are derived from a pool of less differentiated, replicating cells in secondary lymphoid organs, and because IL-2 mediates effector differentiation, the enhanced secondary response may reflect the enlargement of this generative pool by the transient repression of IL-2-mediated differentiation. We have examined for this function the transcriptional repressor BCL6b, a homologue of BCL6 that represses IL-2-induced B cell differentiation. BCL6b is expressed in a small subset of antigen-experienced CD8+ T cells. Ectopic expression of BCL6b in CD8+ T cells diminishes their growth in response to IL-2 in vitro. Female mice in which the BCL6b gene has been interrupted have normal primary responses of CD8+ T cells to infection with vaccinia expressing the H-Y epitope, Uty, but Uty-specific, BCL6 b-/-, memory CD8+ T cells have diminished recall proliferative responses to this epitope in vitro. BCL6 b-/- mice also have normal primary CD8+ T cell responses to influenza infection, but nucleoprotein peptide-specific, BCL6 b-/-, memory CD8+ T cells have a cell autonomous defect in the number of effector cells generated in response to reinfection. Therefore, BCL6b is required for the enhanced magnitude of the secondary response of memory CD8+ T cells. |
| doi_str_mv | 10.1073/pnas.0501585102 |
| format | Article |
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Because effector CD8+ T cells are derived from a pool of less differentiated, replicating cells in secondary lymphoid organs, and because IL-2 mediates effector differentiation, the enhanced secondary response may reflect the enlargement of this generative pool by the transient repression of IL-2-mediated differentiation. We have examined for this function the transcriptional repressor BCL6b, a homologue of BCL6 that represses IL-2-induced B cell differentiation. BCL6b is expressed in a small subset of antigen-experienced CD8+ T cells. Ectopic expression of BCL6b in CD8+ T cells diminishes their growth in response to IL-2 in vitro. Female mice in which the BCL6b gene has been interrupted have normal primary responses of CD8+ T cells to infection with vaccinia expressing the H-Y epitope, Uty, but Uty-specific, BCL6 b-/-, memory CD8+ T cells have diminished recall proliferative responses to this epitope in vitro. BCL6 b-/- mice also have normal primary CD8+ T cell responses to influenza infection, but nucleoprotein peptide-specific, BCL6 b-/-, memory CD8+ T cells have a cell autonomous defect in the number of effector cells generated in response to reinfection. Therefore, BCL6b is required for the enhanced magnitude of the secondary response of memory CD8+ T cells.</description><identifier>ISSN: 0027-8424</identifier><identifier>EISSN: 1091-6490</identifier><identifier>DOI: 10.1073/pnas.0501585102</identifier><identifier>PMID: 15833813</identifier><language>eng</language><publisher>United States: National Academy of Sciences</publisher><subject>Animals ; B lymphocytes ; Biological Sciences ; CD8-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - metabolism ; Cell Differentiation - immunology ; Cell lines ; DNA Primers ; Epitopes - metabolism ; Female ; Gene Components ; Gene Targeting ; Genetic Vectors ; H-Y Antigen - metabolism ; Humans ; Immunologic Memory ; Infections ; Interferon-gamma - metabolism ; Interleukin-2 - immunology ; Interleukin-2 - metabolism ; Lungs ; Lymphoid tissue ; Memory ; Messenger RNA ; Mice ; Mice, Knockout ; Moloney murine leukemia virus ; Repressor Proteins - genetics ; Repressor Proteins - metabolism ; Reverse Transcriptase Polymerase Chain Reaction ; Silencer Elements, Transcriptional - immunology ; T lymphocytes ; Vaccinia - immunology</subject><ispartof>Proceedings of the National Academy of Sciences - PNAS, 2005-05, Vol.102 (21), p.7418-7425</ispartof><rights>Copyright 1993/2005 The National Academy of Sciences of the United States of America</rights><rights>Copyright © 2005, The National Academy of Sciences 2005</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c469t-380a9ddc82dbc8623656e156af6bd5115e6ff75b16fccf9f8221402aa5a94c3c3</citedby><cites>FETCH-LOGICAL-c469t-380a9ddc82dbc8623656e156af6bd5115e6ff75b16fccf9f8221402aa5a94c3c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Uhttp://www.pnas.org/content/102/21.cover.gif</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/3375550$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/3375550$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,723,776,780,799,881,27901,27902,53766,53768,57992,58225</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15833813$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Manders, Peter M.</creatorcontrib><creatorcontrib>Hunter, Patricia J.</creatorcontrib><creatorcontrib>Telaranta, Aino I.</creatorcontrib><creatorcontrib>Carr, James M.</creatorcontrib><creatorcontrib>Marshall, Jennifer L.</creatorcontrib><creatorcontrib>Carrasco, Marlene</creatorcontrib><creatorcontrib>Murakami, Yusuke</creatorcontrib><creatorcontrib>Palmowski, Michael J.</creatorcontrib><creatorcontrib>Cerundolo, Vincenzo</creatorcontrib><creatorcontrib>Kaech, Susan M.</creatorcontrib><creatorcontrib>Ahmed, Rafi</creatorcontrib><creatorcontrib>Fearon, Douglas T.</creatorcontrib><title>BCL6b Mediates the Enhanced Magnitude of the Secondary Response of Memory CD8+ T Lymphocytes</title><title>Proceedings of the National Academy of Sciences - PNAS</title><addtitle>Proc Natl Acad Sci U S A</addtitle><description>A characteristic of the secondary response of CD8+ T cells that distinguishes it from the primary response is the generation of greater numbers of effector cells. Because effector CD8+ T cells are derived from a pool of less differentiated, replicating cells in secondary lymphoid organs, and because IL-2 mediates effector differentiation, the enhanced secondary response may reflect the enlargement of this generative pool by the transient repression of IL-2-mediated differentiation. We have examined for this function the transcriptional repressor BCL6b, a homologue of BCL6 that represses IL-2-induced B cell differentiation. BCL6b is expressed in a small subset of antigen-experienced CD8+ T cells. Ectopic expression of BCL6b in CD8+ T cells diminishes their growth in response to IL-2 in vitro. Female mice in which the BCL6b gene has been interrupted have normal primary responses of CD8+ T cells to infection with vaccinia expressing the H-Y epitope, Uty, but Uty-specific, BCL6 b-/-, memory CD8+ T cells have diminished recall proliferative responses to this epitope in vitro. BCL6 b-/- mice also have normal primary CD8+ T cell responses to influenza infection, but nucleoprotein peptide-specific, BCL6 b-/-, memory CD8+ T cells have a cell autonomous defect in the number of effector cells generated in response to reinfection. Therefore, BCL6b is required for the enhanced magnitude of the secondary response of memory CD8+ T cells.</description><subject>Animals</subject><subject>B lymphocytes</subject><subject>Biological Sciences</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>Cell Differentiation - immunology</subject><subject>Cell lines</subject><subject>DNA Primers</subject><subject>Epitopes - metabolism</subject><subject>Female</subject><subject>Gene Components</subject><subject>Gene Targeting</subject><subject>Genetic Vectors</subject><subject>H-Y Antigen - metabolism</subject><subject>Humans</subject><subject>Immunologic Memory</subject><subject>Infections</subject><subject>Interferon-gamma - metabolism</subject><subject>Interleukin-2 - immunology</subject><subject>Interleukin-2 - metabolism</subject><subject>Lungs</subject><subject>Lymphoid tissue</subject><subject>Memory</subject><subject>Messenger RNA</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Moloney murine leukemia virus</subject><subject>Repressor Proteins - genetics</subject><subject>Repressor Proteins - metabolism</subject><subject>Reverse Transcriptase Polymerase Chain Reaction</subject><subject>Silencer Elements, Transcriptional - immunology</subject><subject>T lymphocytes</subject><subject>Vaccinia - immunology</subject><issn>0027-8424</issn><issn>1091-6490</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kV1rFDEUhoModlu99kZ0roog0-ZjksncCLrWD9hF0HonhExy0p0yk4yTjLj_3mx36eqNV4FznvPkhRehZwRfEFyzy9HreIE5JlxygukDtCC4IaWoGvwQLTCmdSkrWp2g0xhvMcYNl_gxOsk4Y5KwBfrxbrkSbbEG2-kEsUgbKK78RnsDtljrG9-l2UIR3N3mG5jgrZ62xVeIY_DxbrOGIeTR8r18XVwXq-0wboLZZtsT9MjpPsLTw3uGvn-4ul5-KldfPn5evl2VphJNKpnEurHWSGpbIwVlggsgXGgnWssJ4SCcq3lLhDPGNU5SSipMtea6qQwz7Ay92XvHuR3AGvBp0r0ap27IWVXQnfp347uNugm_FMmeipEsOD8IpvBzhpjU0EUDfa89hDkqUUtRc15n8HIPminEOIG7_4RgtWtE7RpRx0byxYu_sx35QwUZeHUAdpdHHVWUqLoiUrm57xP8Thl9-X80E8_3xG1MYbpHGMvpOWZ_ANdnqSY</recordid><startdate>20050524</startdate><enddate>20050524</enddate><creator>Manders, Peter M.</creator><creator>Hunter, Patricia J.</creator><creator>Telaranta, Aino I.</creator><creator>Carr, James M.</creator><creator>Marshall, Jennifer L.</creator><creator>Carrasco, Marlene</creator><creator>Murakami, Yusuke</creator><creator>Palmowski, Michael J.</creator><creator>Cerundolo, Vincenzo</creator><creator>Kaech, Susan M.</creator><creator>Ahmed, Rafi</creator><creator>Fearon, Douglas T.</creator><general>National Academy of Sciences</general><general>National Acad Sciences</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>7X8</scope><scope>5PM</scope></search><sort><creationdate>20050524</creationdate><title>BCL6b Mediates the Enhanced Magnitude of the Secondary Response of Memory CD8+ T Lymphocytes</title><author>Manders, Peter M. ; 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Because effector CD8+ T cells are derived from a pool of less differentiated, replicating cells in secondary lymphoid organs, and because IL-2 mediates effector differentiation, the enhanced secondary response may reflect the enlargement of this generative pool by the transient repression of IL-2-mediated differentiation. We have examined for this function the transcriptional repressor BCL6b, a homologue of BCL6 that represses IL-2-induced B cell differentiation. BCL6b is expressed in a small subset of antigen-experienced CD8+ T cells. Ectopic expression of BCL6b in CD8+ T cells diminishes their growth in response to IL-2 in vitro. Female mice in which the BCL6b gene has been interrupted have normal primary responses of CD8+ T cells to infection with vaccinia expressing the H-Y epitope, Uty, but Uty-specific, BCL6 b-/-, memory CD8+ T cells have diminished recall proliferative responses to this epitope in vitro. BCL6 b-/- mice also have normal primary CD8+ T cell responses to influenza infection, but nucleoprotein peptide-specific, BCL6 b-/-, memory CD8+ T cells have a cell autonomous defect in the number of effector cells generated in response to reinfection. Therefore, BCL6b is required for the enhanced magnitude of the secondary response of memory CD8+ T cells.</abstract><cop>United States</cop><pub>National Academy of Sciences</pub><pmid>15833813</pmid><doi>10.1073/pnas.0501585102</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals B lymphocytes Biological Sciences CD8-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - metabolism Cell Differentiation - immunology Cell lines DNA Primers Epitopes - metabolism Female Gene Components Gene Targeting Genetic Vectors H-Y Antigen - metabolism Humans Immunologic Memory Infections Interferon-gamma - metabolism Interleukin-2 - immunology Interleukin-2 - metabolism Lungs Lymphoid tissue Memory Messenger RNA Mice Mice, Knockout Moloney murine leukemia virus Repressor Proteins - genetics Repressor Proteins - metabolism Reverse Transcriptase Polymerase Chain Reaction Silencer Elements, Transcriptional - immunology T lymphocytes Vaccinia - immunology |
| title | BCL6b Mediates the Enhanced Magnitude of the Secondary Response of Memory CD8+ T Lymphocytes |
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