Enhanced neointima formation following arterial injury in immune deficient Rag-1-/- mice is attenuated by adoptive transfer of CD8 T cells
T cells modulate neointima formation after arterial injury but the specific T cell population that is activated in response to arterial injury remains unknown. The objective of the study was to identify the T cell populations that are activated and modulate neointimal thickening after arterial injur...
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description | T cells modulate neointima formation after arterial injury but the specific T cell population that is activated in response to arterial injury remains unknown. The objective of the study was to identify the T cell populations that are activated and modulate neointimal thickening after arterial injury in mice. Arterial injury in wild type C57Bl6 mice resulted in T cell activation characterized by increased CD4(+)CD44(hi) and CD8(+)CD44(hi) T cells in the lymph nodes and spleens. Splenic CD8(+)CD25(+) T cells and CD8(+)CD28(+) T cells, but not CD4(+)CD25(+) and CD4(+)CD28(+) T cells, were also significantly increased. Adoptive cell transfer of CD4(+) or CD8(+) T cells from donor CD8-/- or CD4-/- mice, respectively, to immune-deficient Rag-1-/- mice was performed to determine the T cell subtype that inhibits neointima formation after arterial injury. Rag-1-/- mice that received CD8(+) T cells had significantly reduced neointima formation compared with Rag-1-/- mice without cell transfer. CD4(+) T cell transfer did not reduce neointima formation. CD8(+) T cells from CD4-/- mice had cytotoxic activity against syngeneic smooth muscle cells in vitro. The study shows that although both CD8(+) T cells and CD4(+) T cells are activated in response to arterial injury, adoptive cell transfer identifies CD8(+) T cells as the specific and selective cell type involved in inhibiting neointima formation. |
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The objective of the study was to identify the T cell populations that are activated and modulate neointimal thickening after arterial injury in mice. Arterial injury in wild type C57Bl6 mice resulted in T cell activation characterized by increased CD4(+)CD44(hi) and CD8(+)CD44(hi) T cells in the lymph nodes and spleens. Splenic CD8(+)CD25(+) T cells and CD8(+)CD28(+) T cells, but not CD4(+)CD25(+) and CD4(+)CD28(+) T cells, were also significantly increased. Adoptive cell transfer of CD4(+) or CD8(+) T cells from donor CD8-/- or CD4-/- mice, respectively, to immune-deficient Rag-1-/- mice was performed to determine the T cell subtype that inhibits neointima formation after arterial injury. Rag-1-/- mice that received CD8(+) T cells had significantly reduced neointima formation compared with Rag-1-/- mice without cell transfer. CD4(+) T cell transfer did not reduce neointima formation. CD8(+) T cells from CD4-/- mice had cytotoxic activity against syngeneic smooth muscle cells in vitro. The study shows that although both CD8(+) T cells and CD4(+) T cells are activated in response to arterial injury, adoptive cell transfer identifies CD8(+) T cells as the specific and selective cell type involved in inhibiting neointima formation.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0020214</identifier><identifier>PMID: 21629656</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adoptive Transfer ; Animals ; Apolipoproteins ; Atherosclerosis ; Biology ; Cardiology ; Carotid Arteries - pathology ; CD25 antigen ; CD28 antigen ; CD4 antigen ; CD4-Positive T-Lymphocytes - metabolism ; CD8 antigen ; CD8-Positive T-Lymphocytes - metabolism ; Cell activation ; Cytotoxicity ; Flow Cytometry ; Heart ; Homeodomain Proteins - genetics ; Homeodomain Proteins - metabolism ; Hypoxia ; Immunohistochemistry ; In Vitro Techniques ; Inflammation ; Injury prevention ; Lymph nodes ; Lymphatic system ; Lymphocytes ; Lymphocytes T ; Male ; Medicine ; Mice ; Mice, Mutant Strains ; Neointima - immunology ; Nitric oxide ; Rodents ; Smooth muscle ; Spleen ; T cell receptors ; Thickening</subject><ispartof>PloS one, 2011, Vol.6 (5), p.e20214-e20214</ispartof><rights>2011 Dimayuga et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Dimayuga et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-b933531355ffa7222caaf0e4f750a1a70f6fcee1f761c8f2b2a887107f6bdfa73</citedby><cites>FETCH-LOGICAL-c525t-b933531355ffa7222caaf0e4f750a1a70f6fcee1f761c8f2b2a887107f6bdfa73</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3101237/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3101237/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,4024,23866,27923,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21629656$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zernecke, Alma</contributor><creatorcontrib>Dimayuga, Paul C</creatorcontrib><creatorcontrib>Chyu, Kuang-Yuh</creatorcontrib><creatorcontrib>Kirzner, Jonathan</creatorcontrib><creatorcontrib>Yano, Juliana</creatorcontrib><creatorcontrib>Zhao, Xiaoning</creatorcontrib><creatorcontrib>Zhou, Jianchang</creatorcontrib><creatorcontrib>Shah, Prediman K</creatorcontrib><creatorcontrib>Cercek, Bojan</creatorcontrib><title>Enhanced neointima formation following arterial injury in immune deficient Rag-1-/- mice is attenuated by adoptive transfer of CD8 T cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>T cells modulate neointima formation after arterial injury but the specific T cell population that is activated in response to arterial injury remains unknown. The objective of the study was to identify the T cell populations that are activated and modulate neointimal thickening after arterial injury in mice. Arterial injury in wild type C57Bl6 mice resulted in T cell activation characterized by increased CD4(+)CD44(hi) and CD8(+)CD44(hi) T cells in the lymph nodes and spleens. Splenic CD8(+)CD25(+) T cells and CD8(+)CD28(+) T cells, but not CD4(+)CD25(+) and CD4(+)CD28(+) T cells, were also significantly increased. Adoptive cell transfer of CD4(+) or CD8(+) T cells from donor CD8-/- or CD4-/- mice, respectively, to immune-deficient Rag-1-/- mice was performed to determine the T cell subtype that inhibits neointima formation after arterial injury. Rag-1-/- mice that received CD8(+) T cells had significantly reduced neointima formation compared with Rag-1-/- mice without cell transfer. CD4(+) T cell transfer did not reduce neointima formation. CD8(+) T cells from CD4-/- mice had cytotoxic activity against syngeneic smooth muscle cells in vitro. The study shows that although both CD8(+) T cells and CD4(+) T cells are activated in response to arterial injury, adoptive cell transfer identifies CD8(+) T cells as the specific and selective cell type involved in inhibiting neointima formation.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Apolipoproteins</subject><subject>Atherosclerosis</subject><subject>Biology</subject><subject>Cardiology</subject><subject>Carotid Arteries - pathology</subject><subject>CD25 antigen</subject><subject>CD28 antigen</subject><subject>CD4 antigen</subject><subject>CD4-Positive T-Lymphocytes - metabolism</subject><subject>CD8 antigen</subject><subject>CD8-Positive T-Lymphocytes - metabolism</subject><subject>Cell activation</subject><subject>Cytotoxicity</subject><subject>Flow Cytometry</subject><subject>Heart</subject><subject>Homeodomain Proteins - genetics</subject><subject>Homeodomain Proteins - metabolism</subject><subject>Hypoxia</subject><subject>Immunohistochemistry</subject><subject>In Vitro Techniques</subject><subject>Inflammation</subject><subject>Injury prevention</subject><subject>Lymph nodes</subject><subject>Lymphatic system</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Male</subject><subject>Medicine</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Neointima - immunology</subject><subject>Nitric oxide</subject><subject>Rodents</subject><subject>Smooth muscle</subject><subject>Spleen</subject><subject>T cell receptors</subject><subject>Thickening</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUl1rFDEUHUSxtfoPRAM--DTbfEySmRdB1qqFgiD1OdzJJNssM8maZCr7F_zVZtxtacWne0nOObn35FTVa4JXhElyvg1z9DCudsGbFcYUU9I8qU5Jx2gtKGZPH_Qn1YuUthhz1grxvDqhRNBOcHFa_b7wN-C1GZA3wfnsJkA2xAmyC7504xh-Ob9BELOJDkbk_HaO-1KQm6bZGzQY67QzPqPvsKlJfV6jyWmDXEKQs_Ez5KLe7xEMYZfdrUE5gk_WRBQsWn9q0TXSZhzTy-qZhTGZV8d6Vv34fHG9_lpffftyuf54VWtOea77jjHOCOPcWpCUUg1gsWms5BgISGyF1cYQKwXRraU9hbaVBEsr-qEw2Fn19qC7G0NSRxuTIrRredcIsSAuD4ghwFbtYjEl7lUAp_4ehLhRxQ-nR6NYZzHuLeFlqGbQppOW8a6XXGpJBIai9eH42txPpiB8WX98JPr4xrsbtQm3ihFMKFuGeX8UiOHnbFJWk0uLYVB-bE6qFZ3sZNPygnz3D_L_yzUHlI4hpWjs_SwEqyVZdyy1JEsdk1Vobx7ucU-6ixL7A9Nszc8</recordid><startdate>2011</startdate><enddate>2011</enddate><creator>Dimayuga, Paul C</creator><creator>Chyu, Kuang-Yuh</creator><creator>Kirzner, Jonathan</creator><creator>Yano, Juliana</creator><creator>Zhao, Xiaoning</creator><creator>Zhou, Jianchang</creator><creator>Shah, Prediman K</creator><creator>Cercek, Bojan</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>2011</creationdate><title>Enhanced neointima formation following arterial injury in immune deficient Rag-1-/- mice is attenuated by adoptive transfer of CD8 T cells</title><author>Dimayuga, Paul C ; Chyu, Kuang-Yuh ; Kirzner, Jonathan ; Yano, Juliana ; Zhao, Xiaoning ; Zhou, Jianchang ; Shah, Prediman K ; Cercek, Bojan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-b933531355ffa7222caaf0e4f750a1a70f6fcee1f761c8f2b2a887107f6bdfa73</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Apolipoproteins</topic><topic>Atherosclerosis</topic><topic>Biology</topic><topic>Cardiology</topic><topic>Carotid Arteries - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dimayuga, Paul C</au><au>Chyu, Kuang-Yuh</au><au>Kirzner, Jonathan</au><au>Yano, Juliana</au><au>Zhao, Xiaoning</au><au>Zhou, Jianchang</au><au>Shah, Prediman K</au><au>Cercek, Bojan</au><au>Zernecke, Alma</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Enhanced neointima formation following arterial injury in immune deficient Rag-1-/- mice is attenuated by adoptive transfer of CD8 T cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011</date><risdate>2011</risdate><volume>6</volume><issue>5</issue><spage>e20214</spage><epage>e20214</epage><pages>e20214-e20214</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>T cells modulate neointima formation after arterial injury but the specific T cell population that is activated in response to arterial injury remains unknown. The objective of the study was to identify the T cell populations that are activated and modulate neointimal thickening after arterial injury in mice. Arterial injury in wild type C57Bl6 mice resulted in T cell activation characterized by increased CD4(+)CD44(hi) and CD8(+)CD44(hi) T cells in the lymph nodes and spleens. Splenic CD8(+)CD25(+) T cells and CD8(+)CD28(+) T cells, but not CD4(+)CD25(+) and CD4(+)CD28(+) T cells, were also significantly increased. Adoptive cell transfer of CD4(+) or CD8(+) T cells from donor CD8-/- or CD4-/- mice, respectively, to immune-deficient Rag-1-/- mice was performed to determine the T cell subtype that inhibits neointima formation after arterial injury. Rag-1-/- mice that received CD8(+) T cells had significantly reduced neointima formation compared with Rag-1-/- mice without cell transfer. CD4(+) T cell transfer did not reduce neointima formation. CD8(+) T cells from CD4-/- mice had cytotoxic activity against syngeneic smooth muscle cells in vitro. The study shows that although both CD8(+) T cells and CD4(+) T cells are activated in response to arterial injury, adoptive cell transfer identifies CD8(+) T cells as the specific and selective cell type involved in inhibiting neointima formation.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21629656</pmid><doi>10.1371/journal.pone.0020214</doi><oa>free_for_read</oa></addata></record> |
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subjects | Adoptive Transfer Animals Apolipoproteins Atherosclerosis Biology Cardiology Carotid Arteries - pathology CD25 antigen CD28 antigen CD4 antigen CD4-Positive T-Lymphocytes - metabolism CD8 antigen CD8-Positive T-Lymphocytes - metabolism Cell activation Cytotoxicity Flow Cytometry Heart Homeodomain Proteins - genetics Homeodomain Proteins - metabolism Hypoxia Immunohistochemistry In Vitro Techniques Inflammation Injury prevention Lymph nodes Lymphatic system Lymphocytes Lymphocytes T Male Medicine Mice Mice, Mutant Strains Neointima - immunology Nitric oxide Rodents Smooth muscle Spleen T cell receptors Thickening |
title | Enhanced neointima formation following arterial injury in immune deficient Rag-1-/- mice is attenuated by adoptive transfer of CD8 T cells |
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