S1P1 receptor signaling overrides retention mediated by G alpha i-coupled receptors to promote T cell egress
The mechanism by which sphingosine-1-phosphate receptor-1 (S1P1) acts to promote lymphocyte egress from lymphoid organs is not defined. Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. Afte...
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Veröffentlicht in: | Immunity (Cambridge, Mass.) Mass.), 2008-01, Vol.28 (1), p.122-133 |
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description | The mechanism by which sphingosine-1-phosphate receptor-1 (S1P1) acts to promote lymphocyte egress from lymphoid organs is not defined. Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. After treatment with FTY720, an agonist that causes downmodulation of lymphocyte S1P1, CCR7-deficient T cells were less effectively retained than wild-type T cells. Moreover, treatment with pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress competence to S1P1-deficient lymphocytes. We also found that T cell accumulation in lymph node cortical sinusoids required intrinsic S1P1 expression and was antagonized by CCR7. These findings suggest a model where S1P1 acts in the lymphocyte to promote lymph node egress by overcoming retention signals mediated by CCR7 and additional G alpha i-coupled receptors. Furthermore, by simultaneously upregulating S1P1 and downregulating CCR7, T cells that have divided multiple times switch to a state favoring egress over retention. |
doi_str_mv | 10.1016/j.immuni.2007.11.017 |
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Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. After treatment with FTY720, an agonist that causes downmodulation of lymphocyte S1P1, CCR7-deficient T cells were less effectively retained than wild-type T cells. Moreover, treatment with pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress competence to S1P1-deficient lymphocytes. We also found that T cell accumulation in lymph node cortical sinusoids required intrinsic S1P1 expression and was antagonized by CCR7. These findings suggest a model where S1P1 acts in the lymphocyte to promote lymph node egress by overcoming retention signals mediated by CCR7 and additional G alpha i-coupled receptors. 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Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. After treatment with FTY720, an agonist that causes downmodulation of lymphocyte S1P1, CCR7-deficient T cells were less effectively retained than wild-type T cells. Moreover, treatment with pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress competence to S1P1-deficient lymphocytes. We also found that T cell accumulation in lymph node cortical sinusoids required intrinsic S1P1 expression and was antagonized by CCR7. These findings suggest a model where S1P1 acts in the lymphocyte to promote lymph node egress by overcoming retention signals mediated by CCR7 and additional G alpha i-coupled receptors. Furthermore, by simultaneously upregulating S1P1 and downregulating CCR7, T cells that have divided multiple times switch to a state favoring egress over retention.</description><subject>Adoptive Transfer</subject><subject>Animals</subject><subject>Chemotaxis, Leukocyte - immunology</subject><subject>Flow Cytometry</subject><subject>GTP-Binding Protein alpha Subunit, Gi2 - immunology</subject><subject>GTP-Binding Protein alpha Subunit, Gi2 - metabolism</subject><subject>Immunohistochemistry</subject><subject>Lymph Nodes - cytology</subject><subject>Lymph Nodes - immunology</subject><subject>Lymph Nodes - metabolism</subject><subject>Mice</subject><subject>Mice, Transgenic</subject><subject>Receptors, CCR7 - immunology</subject><subject>Receptors, CCR7 - metabolism</subject><subject>Receptors, Lysosphingolipid - immunology</subject><subject>Receptors, Lysosphingolipid - metabolism</subject><subject>Signal Transduction - immunology</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - metabolism</subject><issn>1074-7613</issn><issn>1097-4180</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU1r3DAQhkVJadK0_6AUnXKzO2PJlnUphJCmhUALTc9CK483WmzLkexA_n207DZNTzPMxzvv8DD2CaFEwObLrvTjuE6-rABUiVgCqjfsDEGrQmILJ_tcyUI1KE7Z-5R2AChrDe_YKbbYyKrCMzb8xl_IIzmalxB58tvJDn7a8vBIMfqOUm4uNC0-THykztuFOr554jfcDvO95b5wYZ2HXPwrkvgS-BzDGBbid9zRMHDaRkrpA3vb2yHRx2M8Z3--Xd9dfS9uf978uLq8LZyoUBW2U64XTd9JbbUWtleCAOoGQdi60-Ra4bpGOqHQtnVNttX5mU7WcqOaDVhxzr4edOd1kz27bD_awczRjzY-mWC9-b8z-XuzDY-majQKDVng4igQw8NKaTGjT_tH7ERhTUZBBbVsZR6Uh0EXQ0qR-pcjCGaPyezMAZPZYzKIJmPKa59fG_y3dOQingHebpKl</recordid><startdate>200801</startdate><enddate>200801</enddate><creator>Pham, Trung H M</creator><creator>Okada, Takaharu</creator><creator>Matloubian, Mehrdad</creator><creator>Lo, Charles G</creator><creator>Cyster, Jason G</creator><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>200801</creationdate><title>S1P1 receptor signaling overrides retention mediated by G alpha i-coupled receptors to promote T cell egress</title><author>Pham, Trung H M ; Okada, Takaharu ; Matloubian, Mehrdad ; Lo, Charles G ; Cyster, Jason G</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3217-ad7cf36fd49a993af73e0056103a5d9ec83cd64c371a855ea89422d454b76b0a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>Adoptive Transfer</topic><topic>Animals</topic><topic>Chemotaxis, Leukocyte - immunology</topic><topic>Flow Cytometry</topic><topic>GTP-Binding Protein alpha Subunit, Gi2 - immunology</topic><topic>GTP-Binding Protein alpha Subunit, Gi2 - metabolism</topic><topic>Immunohistochemistry</topic><topic>Lymph Nodes - cytology</topic><topic>Lymph Nodes - immunology</topic><topic>Lymph Nodes - metabolism</topic><topic>Mice</topic><topic>Mice, Transgenic</topic><topic>Receptors, CCR7 - immunology</topic><topic>Receptors, CCR7 - metabolism</topic><topic>Receptors, Lysosphingolipid - immunology</topic><topic>Receptors, Lysosphingolipid - metabolism</topic><topic>Signal Transduction - immunology</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pham, Trung H M</creatorcontrib><creatorcontrib>Okada, Takaharu</creatorcontrib><creatorcontrib>Matloubian, Mehrdad</creatorcontrib><creatorcontrib>Lo, Charles G</creatorcontrib><creatorcontrib>Cyster, Jason G</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Immunity (Cambridge, Mass.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pham, Trung H M</au><au>Okada, Takaharu</au><au>Matloubian, Mehrdad</au><au>Lo, Charles G</au><au>Cyster, Jason G</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S1P1 receptor signaling overrides retention mediated by G alpha i-coupled receptors to promote T cell egress</atitle><jtitle>Immunity (Cambridge, Mass.)</jtitle><addtitle>Immunity</addtitle><date>2008-01</date><risdate>2008</risdate><volume>28</volume><issue>1</issue><spage>122</spage><epage>133</epage><pages>122-133</pages><issn>1074-7613</issn><eissn>1097-4180</eissn><abstract>The mechanism by which sphingosine-1-phosphate receptor-1 (S1P1) acts to promote lymphocyte egress from lymphoid organs is not defined. Here, we showed that CCR7-deficient T cells left lymph nodes more rapidly than wild-type cells did, whereas CCR7-overexpressing cells were retained for longer. After treatment with FTY720, an agonist that causes downmodulation of lymphocyte S1P1, CCR7-deficient T cells were less effectively retained than wild-type T cells. Moreover, treatment with pertussis toxin to inactivate signaling via G alpha i-protein-coupled receptors restored egress competence to S1P1-deficient lymphocytes. We also found that T cell accumulation in lymph node cortical sinusoids required intrinsic S1P1 expression and was antagonized by CCR7. These findings suggest a model where S1P1 acts in the lymphocyte to promote lymph node egress by overcoming retention signals mediated by CCR7 and additional G alpha i-coupled receptors. 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subjects | Adoptive Transfer Animals Chemotaxis, Leukocyte - immunology Flow Cytometry GTP-Binding Protein alpha Subunit, Gi2 - immunology GTP-Binding Protein alpha Subunit, Gi2 - metabolism Immunohistochemistry Lymph Nodes - cytology Lymph Nodes - immunology Lymph Nodes - metabolism Mice Mice, Transgenic Receptors, CCR7 - immunology Receptors, CCR7 - metabolism Receptors, Lysosphingolipid - immunology Receptors, Lysosphingolipid - metabolism Signal Transduction - immunology T-Lymphocytes - immunology T-Lymphocytes - metabolism |
title | S1P1 receptor signaling overrides retention mediated by G alpha i-coupled receptors to promote T cell egress |
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