CD8 super(+) T Lymphocytes Regulate the Arteriogenic Response to Ischemia by Infiltrating the Site of Collateral Vessel Development and Recruiting CD4 super(+) Mononuclear Cells Through the Expression of Interleukin-16
BACKGROUND: Previous studies have demonstrated that macrophages and CD4 super(+) T lymphocytes play pivotal roles in collateral development. Indirect evidence suggests that CD8 super(+) T cells also play a role. Thus, after acute cerebral ischemia, CD8 super(+) T cells infiltrate the perivascular sp...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2006-01, Vol.113 (1), p.118-124 |
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| creator | Stabile, Eugenio Kinnaird, Timothy la Sala, Andrea Hanson, Sue Kim Watkins, Craig Campia, Umberto Shou, Matie Zbinden, Stephan Fuchs, Shmuel Kornfeld, Hardy Epstein, Stephen E Burnett, Mary Susan |
| description | BACKGROUND: Previous studies have demonstrated that macrophages and CD4 super(+) T lymphocytes play pivotal roles in collateral development. Indirect evidence suggests that CD8 super(+) T cells also play a role. Thus, after acute cerebral ischemia, CD8 super(+) T cells infiltrate the perivascular space and secrete interleukin-16 (IL-16), a potent chemoattractant for monocytes and CD4 super(+) T cells. We tested whether CD8 super(+) T lymphocytes contribute to collateral vessel development and whether the lack of circulating CD8 super(+) T cells prevents IL-16 expression, impairs CD4 super(+) mononuclear cell recruitment, and reduces collateral vessel growth after femoral artery ligation in CD8 super(-/-) mice. METHOD:S: and Results- After surgical excision of the femoral artery, laser Doppler perfusion imaging demonstrated reduced blood flow recovery in CD8 super(-/-) mice compared with C57/BL6 mice (ischemic/nonischemic limb at day 28, 0.66 plus or minus 0.04 versus 0.87 plus or minus 0.04, respectively; P |
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| fullrecord | <record><control><sourceid>proquest</sourceid><recordid>TN_cdi_proquest_miscellaneous_20793335</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>20793335</sourcerecordid><originalsourceid>FETCH-proquest_miscellaneous_207933353</originalsourceid><addsrcrecordid>eNqNjk1Lw0AQhoMoWD_-w5xEkUCaTRp7lKTSgl60eC1rnCSrm524syvmr_pr3AbBq6dheOd53jmIZvM8zeIsF8vDaJYkyTIuRJoeRyfMb2FdiCKfRd9ldQPsB7SX11ewhfuxHzqqR4cMj9h6LR2C6xBurUOrqEWj6pDwQIZDQrDhusNeSXgZYWMapZ2VTpl2op5UwKmBkvTeZKWGZ2RGDRV-oqahR-NAmtegrK1XE1hW2d9LD2TI-FqjtFCi1gzbzpJvu8m_-hps8Cky-5aNCRUa_bsy8XxxFh01UjOe_87T6OJutS3X8WDpwyO7Xa-4DkppkDzv0qRYCiFy8e_DH7LtdJE</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>20793335</pqid></control><display><type>article</type><title>CD8 super(+) T Lymphocytes Regulate the Arteriogenic Response to Ischemia by Infiltrating the Site of Collateral Vessel Development and Recruiting CD4 super(+) Mononuclear Cells Through the Expression of Interleukin-16</title><source>American Heart Association Journals</source><source>Journals@Ovid Complete</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Stabile, Eugenio ; Kinnaird, Timothy ; la Sala, Andrea ; Hanson, Sue Kim ; Watkins, Craig ; Campia, Umberto ; Shou, Matie ; Zbinden, Stephan ; Fuchs, Shmuel ; Kornfeld, Hardy ; Epstein, Stephen E ; Burnett, Mary Susan</creator><creatorcontrib>Stabile, Eugenio ; Kinnaird, Timothy ; la Sala, Andrea ; Hanson, Sue Kim ; Watkins, Craig ; Campia, Umberto ; Shou, Matie ; Zbinden, Stephan ; Fuchs, Shmuel ; Kornfeld, Hardy ; Epstein, Stephen E ; Burnett, Mary Susan</creatorcontrib><description>BACKGROUND: Previous studies have demonstrated that macrophages and CD4 super(+) T lymphocytes play pivotal roles in collateral development. Indirect evidence suggests that CD8 super(+) T cells also play a role. Thus, after acute cerebral ischemia, CD8 super(+) T cells infiltrate the perivascular space and secrete interleukin-16 (IL-16), a potent chemoattractant for monocytes and CD4 super(+) T cells. We tested whether CD8 super(+) T lymphocytes contribute to collateral vessel development and whether the lack of circulating CD8 super(+) T cells prevents IL-16 expression, impairs CD4 super(+) mononuclear cell recruitment, and reduces collateral vessel growth after femoral artery ligation in CD8 super(-/-) mice. METHOD:S: and Results- After surgical excision of the femoral artery, laser Doppler perfusion imaging demonstrated reduced blood flow recovery in CD8 super(-/-) mice compared with C57/BL6 mice (ischemic/nonischemic limb at day 28, 0.66 plus or minus 0.04 versus 0.87 plus or minus 0.04, respectively; P<0.01). This resulted in greater calf muscle atrophy (mean fiber area, 785 plus or minus 68 versus 1067 plus or minus 69 mu m super(2), respectively; P<0.01) and increased fibrotic tissue content (10.8 plus or minus 1.2% versus 7 plus or minus 1%, respectively; P<0.01). Moreover, CD8 super(-/-) mice displayed reduced IL-16 expression and decreased CD4 super(+) T-cell recruitment at the site of collateral vessel development. Exogenous CD8 super(+) T cells, infused into CD8 super(-/-) mice immediately after femoral artery ligation, selectively homed to the ischemic hind limb and expressed IL-16. The restoration of IL-16 expression resulted in significant CD4 super(+) mononuclear cell infiltration of the ischemic limb, faster blood flow recovery, and reduced hindlimb muscle atrophy/fibrosis. When exogenous CD8 super(+) T cells deficient in IL-16 (IL-16 super(-/-)) were infused into CD8 super(-/-) mice immediately after femoral artery ligation, they selectively homed to the ischemic hind limb but were unable to recruit CD4 super(+) mononuclear cells and did not improve blood flow recovery. CONCLUSIONS: These results demonstrate that CD8 super(+) T cells importantly contribute to the early phase of collateral development. After femoral artery ligation, CD8 super(+) T cells infiltrate the site of collateral vessel growth and recruit CD4 super(+) mononuclear cells through the expression of IL-16. Our study provides further evidence of the significant role of the immune system in modulating collateral development in response to peripheral ischemia.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><language>eng</language><ispartof>Circulation (New York, N.Y.), 2006-01, Vol.113 (1), p.118-124</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784</link.rule.ids></links><search><creatorcontrib>Stabile, Eugenio</creatorcontrib><creatorcontrib>Kinnaird, Timothy</creatorcontrib><creatorcontrib>la Sala, Andrea</creatorcontrib><creatorcontrib>Hanson, Sue Kim</creatorcontrib><creatorcontrib>Watkins, Craig</creatorcontrib><creatorcontrib>Campia, Umberto</creatorcontrib><creatorcontrib>Shou, Matie</creatorcontrib><creatorcontrib>Zbinden, Stephan</creatorcontrib><creatorcontrib>Fuchs, Shmuel</creatorcontrib><creatorcontrib>Kornfeld, Hardy</creatorcontrib><creatorcontrib>Epstein, Stephen E</creatorcontrib><creatorcontrib>Burnett, Mary Susan</creatorcontrib><title>CD8 super(+) T Lymphocytes Regulate the Arteriogenic Response to Ischemia by Infiltrating the Site of Collateral Vessel Development and Recruiting CD4 super(+) Mononuclear Cells Through the Expression of Interleukin-16</title><title>Circulation (New York, N.Y.)</title><description>BACKGROUND: Previous studies have demonstrated that macrophages and CD4 super(+) T lymphocytes play pivotal roles in collateral development. Indirect evidence suggests that CD8 super(+) T cells also play a role. Thus, after acute cerebral ischemia, CD8 super(+) T cells infiltrate the perivascular space and secrete interleukin-16 (IL-16), a potent chemoattractant for monocytes and CD4 super(+) T cells. We tested whether CD8 super(+) T lymphocytes contribute to collateral vessel development and whether the lack of circulating CD8 super(+) T cells prevents IL-16 expression, impairs CD4 super(+) mononuclear cell recruitment, and reduces collateral vessel growth after femoral artery ligation in CD8 super(-/-) mice. METHOD:S: and Results- After surgical excision of the femoral artery, laser Doppler perfusion imaging demonstrated reduced blood flow recovery in CD8 super(-/-) mice compared with C57/BL6 mice (ischemic/nonischemic limb at day 28, 0.66 plus or minus 0.04 versus 0.87 plus or minus 0.04, respectively; P<0.01). This resulted in greater calf muscle atrophy (mean fiber area, 785 plus or minus 68 versus 1067 plus or minus 69 mu m super(2), respectively; P<0.01) and increased fibrotic tissue content (10.8 plus or minus 1.2% versus 7 plus or minus 1%, respectively; P<0.01). Moreover, CD8 super(-/-) mice displayed reduced IL-16 expression and decreased CD4 super(+) T-cell recruitment at the site of collateral vessel development. Exogenous CD8 super(+) T cells, infused into CD8 super(-/-) mice immediately after femoral artery ligation, selectively homed to the ischemic hind limb and expressed IL-16. The restoration of IL-16 expression resulted in significant CD4 super(+) mononuclear cell infiltration of the ischemic limb, faster blood flow recovery, and reduced hindlimb muscle atrophy/fibrosis. When exogenous CD8 super(+) T cells deficient in IL-16 (IL-16 super(-/-)) were infused into CD8 super(-/-) mice immediately after femoral artery ligation, they selectively homed to the ischemic hind limb but were unable to recruit CD4 super(+) mononuclear cells and did not improve blood flow recovery. CONCLUSIONS: These results demonstrate that CD8 super(+) T cells importantly contribute to the early phase of collateral development. After femoral artery ligation, CD8 super(+) T cells infiltrate the site of collateral vessel growth and recruit CD4 super(+) mononuclear cells through the expression of IL-16. Our study provides further evidence of the significant role of the immune system in modulating collateral development in response to peripheral ischemia.</description><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><recordid>eNqNjk1Lw0AQhoMoWD_-w5xEkUCaTRp7lKTSgl60eC1rnCSrm524syvmr_pr3AbBq6dheOd53jmIZvM8zeIsF8vDaJYkyTIuRJoeRyfMb2FdiCKfRd9ldQPsB7SX11ewhfuxHzqqR4cMj9h6LR2C6xBurUOrqEWj6pDwQIZDQrDhusNeSXgZYWMapZ2VTpl2op5UwKmBkvTeZKWGZ2RGDRV-oqahR-NAmtegrK1XE1hW2d9LD2TI-FqjtFCi1gzbzpJvu8m_-hps8Cky-5aNCRUa_bsy8XxxFh01UjOe_87T6OJutS3X8WDpwyO7Xa-4DkppkDzv0qRYCiFy8e_DH7LtdJE</recordid><startdate>20060103</startdate><enddate>20060103</enddate><creator>Stabile, Eugenio</creator><creator>Kinnaird, Timothy</creator><creator>la Sala, Andrea</creator><creator>Hanson, Sue Kim</creator><creator>Watkins, Craig</creator><creator>Campia, Umberto</creator><creator>Shou, Matie</creator><creator>Zbinden, Stephan</creator><creator>Fuchs, Shmuel</creator><creator>Kornfeld, Hardy</creator><creator>Epstein, Stephen E</creator><creator>Burnett, Mary Susan</creator><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>20060103</creationdate><title>CD8 super(+) T Lymphocytes Regulate the Arteriogenic Response to Ischemia by Infiltrating the Site of Collateral Vessel Development and Recruiting CD4 super(+) Mononuclear Cells Through the Expression of Interleukin-16</title><author>Stabile, Eugenio ; Kinnaird, Timothy ; la Sala, Andrea ; Hanson, Sue Kim ; Watkins, Craig ; Campia, Umberto ; Shou, Matie ; Zbinden, Stephan ; Fuchs, Shmuel ; Kornfeld, Hardy ; Epstein, Stephen E ; Burnett, Mary Susan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-proquest_miscellaneous_207933353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Stabile, Eugenio</creatorcontrib><creatorcontrib>Kinnaird, Timothy</creatorcontrib><creatorcontrib>la Sala, Andrea</creatorcontrib><creatorcontrib>Hanson, Sue Kim</creatorcontrib><creatorcontrib>Watkins, Craig</creatorcontrib><creatorcontrib>Campia, Umberto</creatorcontrib><creatorcontrib>Shou, Matie</creatorcontrib><creatorcontrib>Zbinden, Stephan</creatorcontrib><creatorcontrib>Fuchs, Shmuel</creatorcontrib><creatorcontrib>Kornfeld, Hardy</creatorcontrib><creatorcontrib>Epstein, Stephen E</creatorcontrib><creatorcontrib>Burnett, Mary Susan</creatorcontrib><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Stabile, Eugenio</au><au>Kinnaird, Timothy</au><au>la Sala, Andrea</au><au>Hanson, Sue Kim</au><au>Watkins, Craig</au><au>Campia, Umberto</au><au>Shou, Matie</au><au>Zbinden, Stephan</au><au>Fuchs, Shmuel</au><au>Kornfeld, Hardy</au><au>Epstein, Stephen E</au><au>Burnett, Mary Susan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CD8 super(+) T Lymphocytes Regulate the Arteriogenic Response to Ischemia by Infiltrating the Site of Collateral Vessel Development and Recruiting CD4 super(+) Mononuclear Cells Through the Expression of Interleukin-16</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><date>2006-01-03</date><risdate>2006</risdate><volume>113</volume><issue>1</issue><spage>118</spage><epage>124</epage><pages>118-124</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><abstract>BACKGROUND: Previous studies have demonstrated that macrophages and CD4 super(+) T lymphocytes play pivotal roles in collateral development. Indirect evidence suggests that CD8 super(+) T cells also play a role. Thus, after acute cerebral ischemia, CD8 super(+) T cells infiltrate the perivascular space and secrete interleukin-16 (IL-16), a potent chemoattractant for monocytes and CD4 super(+) T cells. We tested whether CD8 super(+) T lymphocytes contribute to collateral vessel development and whether the lack of circulating CD8 super(+) T cells prevents IL-16 expression, impairs CD4 super(+) mononuclear cell recruitment, and reduces collateral vessel growth after femoral artery ligation in CD8 super(-/-) mice. METHOD:S: and Results- After surgical excision of the femoral artery, laser Doppler perfusion imaging demonstrated reduced blood flow recovery in CD8 super(-/-) mice compared with C57/BL6 mice (ischemic/nonischemic limb at day 28, 0.66 plus or minus 0.04 versus 0.87 plus or minus 0.04, respectively; P<0.01). This resulted in greater calf muscle atrophy (mean fiber area, 785 plus or minus 68 versus 1067 plus or minus 69 mu m super(2), respectively; P<0.01) and increased fibrotic tissue content (10.8 plus or minus 1.2% versus 7 plus or minus 1%, respectively; P<0.01). Moreover, CD8 super(-/-) mice displayed reduced IL-16 expression and decreased CD4 super(+) T-cell recruitment at the site of collateral vessel development. Exogenous CD8 super(+) T cells, infused into CD8 super(-/-) mice immediately after femoral artery ligation, selectively homed to the ischemic hind limb and expressed IL-16. The restoration of IL-16 expression resulted in significant CD4 super(+) mononuclear cell infiltration of the ischemic limb, faster blood flow recovery, and reduced hindlimb muscle atrophy/fibrosis. When exogenous CD8 super(+) T cells deficient in IL-16 (IL-16 super(-/-)) were infused into CD8 super(-/-) mice immediately after femoral artery ligation, they selectively homed to the ischemic hind limb but were unable to recruit CD4 super(+) mononuclear cells and did not improve blood flow recovery. CONCLUSIONS: These results demonstrate that CD8 super(+) T cells importantly contribute to the early phase of collateral development. After femoral artery ligation, CD8 super(+) T cells infiltrate the site of collateral vessel growth and recruit CD4 super(+) mononuclear cells through the expression of IL-16. Our study provides further evidence of the significant role of the immune system in modulating collateral development in response to peripheral ischemia.</abstract></addata></record> |
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| title | CD8 super(+) T Lymphocytes Regulate the Arteriogenic Response to Ischemia by Infiltrating the Site of Collateral Vessel Development and Recruiting CD4 super(+) Mononuclear Cells Through the Expression of Interleukin-16 |
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