CXCR3 is required for migration to dermal inflammation by normal and in vivo activated T cells: differential requirements by CD4 and CD8 memory subsets
Lymphocytes in inflamed tissues express numerous chemokine receptors. The relative importance of these receptors for migration in inflammation is unclear. The role of CXCR3 in T cell subset migration was examined using monoclonal antibodies developed to rat CXCR3. CXCR3 was expressed on sixfold more...
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| Veröffentlicht in: | European journal of immunology 2005-06, Vol.35 (6), p.1702-1711 |
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| creator | Mohan, Karkada Cordeiro, Erin Vaci, Maria McMaster, Christopher Issekutz, Thomas B. |
| description | Lymphocytes in inflamed tissues express numerous chemokine receptors. The relative importance of these receptors for migration in inflammation is unclear. The role of CXCR3 in T cell subset migration was examined using monoclonal antibodies developed to rat CXCR3. CXCR3 was expressed on sixfold more CD8+ (∼30%) than CD4+ (∼5%) T cells in spleen, lymph nodes and blood, and on ∼10% of CD4+CD45RC– (memory) and ∼50% of CD8+CD45RC+ spleen T cells. After immunization, CXCR3 increased tenfold on CD4+ lymph node lymphoblasts (∼55%), and >90% of inflammatory exudate T cells were CXCR3+. CXCR3+ T cells migrated significantly better than CXCR3– T cells to all dermal inflammatory stimuli tested in vivo, even though these T cells are a minority of the memory T cells. Blocking CXCR3 inhibited recruitment of 60–85% of unstimulated T cells and up to 90% of CD8+CD45RC+ effector T cells, but caused |
| doi_str_mv | 10.1002/eji.200425885 |
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The relative importance of these receptors for migration in inflammation is unclear. The role of CXCR3 in T cell subset migration was examined using monoclonal antibodies developed to rat CXCR3. CXCR3 was expressed on sixfold more CD8+ (∼30%) than CD4+ (∼5%) T cells in spleen, lymph nodes and blood, and on ∼10% of CD4+CD45RC– (memory) and ∼50% of CD8+CD45RC+ spleen T cells. After immunization, CXCR3 increased tenfold on CD4+ lymph node lymphoblasts (∼55%), and >90% of inflammatory exudate T cells were CXCR3+. CXCR3+ T cells migrated significantly better than CXCR3– T cells to all dermal inflammatory stimuli tested in vivo, even though these T cells are a minority of the memory T cells. Blocking CXCR3 inhibited recruitment of 60–85% of unstimulated T cells and up to 90% of CD8+CD45RC+ effector T cells, but caused <50% inhibition of CD4+ and CD8+ memory (CD45RC–) T cells. About 90% of T lymphoblast migration to IFN‐γ, IFN‐γ plus TNF‐α, polyinosinic polycytidylic acid, lipopolysaccharide, and delayed‐type hypersensitivity (DTH)‐induced inflammation was inhibited. Blockade also reduced DTH‐induced induration. Thus, CXCR3 has a non‐redundant role in T cell migration to dermal inflammation and is critical for activated T lymphoblast recruitment, but memory T cells are less dependent on CXCR3 for their infiltration.</description><identifier>ISSN: 0014-2980</identifier><identifier>EISSN: 1521-4141</identifier><identifier>DOI: 10.1002/eji.200425885</identifier><identifier>PMID: 15884054</identifier><language>eng</language><publisher>Weinheim: WILEY‐VCH Verlag</publisher><subject>Animals ; CD4-Positive T-Lymphocytes - immunology ; CD8-Positive T-Lymphocytes - immunology ; Cell Adhesion ; Cell Movement ; Cell trafficking ; Chemokines ; Chemotaxis, Leukocyte ; CHO Cells ; Cricetinae ; CXCR3 ; Dermatitis - immunology ; Hypersensitivity, Delayed - immunology ; Immunologic Memory ; Inflammation ; Lymphocyte Activation ; Mice ; Receptors, Chemokine - analysis ; Receptors, Chemokine - physiology ; Receptors, CXCR3 ; Spleen - immunology ; T cell</subject><ispartof>European journal of immunology, 2005-06, Vol.35 (6), p.1702-1711</ispartof><rights>Copyright © 2005 WILEY‐VCH Verlag GmbH & Co. KGaA, Weinheim</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1002%2Feji.200425885$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1002%2Feji.200425885$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1416,1432,27923,27924,45573,45574,46408,46832</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15884054$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mohan, Karkada</creatorcontrib><creatorcontrib>Cordeiro, Erin</creatorcontrib><creatorcontrib>Vaci, Maria</creatorcontrib><creatorcontrib>McMaster, Christopher</creatorcontrib><creatorcontrib>Issekutz, Thomas B.</creatorcontrib><title>CXCR3 is required for migration to dermal inflammation by normal and in vivo activated T cells: differential requirements by CD4 and CD8 memory subsets</title><title>European journal of immunology</title><addtitle>Eur J Immunol</addtitle><description>Lymphocytes in inflamed tissues express numerous chemokine receptors. The relative importance of these receptors for migration in inflammation is unclear. The role of CXCR3 in T cell subset migration was examined using monoclonal antibodies developed to rat CXCR3. CXCR3 was expressed on sixfold more CD8+ (∼30%) than CD4+ (∼5%) T cells in spleen, lymph nodes and blood, and on ∼10% of CD4+CD45RC– (memory) and ∼50% of CD8+CD45RC+ spleen T cells. After immunization, CXCR3 increased tenfold on CD4+ lymph node lymphoblasts (∼55%), and >90% of inflammatory exudate T cells were CXCR3+. CXCR3+ T cells migrated significantly better than CXCR3– T cells to all dermal inflammatory stimuli tested in vivo, even though these T cells are a minority of the memory T cells. Blocking CXCR3 inhibited recruitment of 60–85% of unstimulated T cells and up to 90% of CD8+CD45RC+ effector T cells, but caused <50% inhibition of CD4+ and CD8+ memory (CD45RC–) T cells. About 90% of T lymphoblast migration to IFN‐γ, IFN‐γ plus TNF‐α, polyinosinic polycytidylic acid, lipopolysaccharide, and delayed‐type hypersensitivity (DTH)‐induced inflammation was inhibited. Blockade also reduced DTH‐induced induration. Thus, CXCR3 has a non‐redundant role in T cell migration to dermal inflammation and is critical for activated T lymphoblast recruitment, but memory T cells are less dependent on CXCR3 for their infiltration.</description><subject>Animals</subject><subject>CD4-Positive T-Lymphocytes - immunology</subject><subject>CD8-Positive T-Lymphocytes - immunology</subject><subject>Cell Adhesion</subject><subject>Cell Movement</subject><subject>Cell trafficking</subject><subject>Chemokines</subject><subject>Chemotaxis, Leukocyte</subject><subject>CHO Cells</subject><subject>Cricetinae</subject><subject>CXCR3</subject><subject>Dermatitis - immunology</subject><subject>Hypersensitivity, Delayed - immunology</subject><subject>Immunologic Memory</subject><subject>Inflammation</subject><subject>Lymphocyte Activation</subject><subject>Mice</subject><subject>Receptors, Chemokine - analysis</subject><subject>Receptors, Chemokine - physiology</subject><subject>Receptors, CXCR3</subject><subject>Spleen - immunology</subject><subject>T cell</subject><issn>0014-2980</issn><issn>1521-4141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc9u1DAQxi1ERZfCkSvyiVvK2LETmxtKC7SqVAkViVvkxGPkKk62drLV3jjwErweT4K3uy1HTqOZ-embPx8hbxicMgD-Hm_9KQcQXColn5EVk5wVggn2nKwAmCi4VnBMXqZ0CwC6kvoFOWYZFiDFivxuvjdfS-oTjXi3-IiWuinS4H9EM_tppPNELcZgBupHN5gQ9uVuS8fpoWxGm1t04zcTNf3sN2bOIjd_fv7qcRjSB2q9cxhxnH2mD1NCTtNOpDkTDwrNmaIBwxS3NC1dwjm9IkfODAlfH-IJ-fbp_Kb5Ulxdf75oPl4Va54vLvpeSumstRK7Sri6cqoGRMs0CsF4XVqG2oBWneilLvPhnLvaKFHr3gopyxPybq-7jtPdgmlug0-71c2I05LaSgFTVQn_BVmt6qrSO_DtAVy6gLZdRx9M3LaPX89AvQfu_YDbf31od5a22dL2ydL2_PLiKSn_AqHElko</recordid><startdate>200506</startdate><enddate>200506</enddate><creator>Mohan, Karkada</creator><creator>Cordeiro, Erin</creator><creator>Vaci, Maria</creator><creator>McMaster, Christopher</creator><creator>Issekutz, Thomas B.</creator><general>WILEY‐VCH Verlag</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>200506</creationdate><title>CXCR3 is required for migration to dermal inflammation by normal and in vivo activated T cells: differential requirements by CD4 and CD8 memory subsets</title><author>Mohan, Karkada ; Cordeiro, Erin ; Vaci, Maria ; McMaster, Christopher ; Issekutz, Thomas B.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p2885-cc555fddd5eb64f76f870eed19e441273d1e9a098b4c59358822f7a8479cd4553</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>CD4-Positive T-Lymphocytes - immunology</topic><topic>CD8-Positive T-Lymphocytes - immunology</topic><topic>Cell Adhesion</topic><topic>Cell Movement</topic><topic>Cell trafficking</topic><topic>Chemokines</topic><topic>Chemotaxis, Leukocyte</topic><topic>CHO Cells</topic><topic>Cricetinae</topic><topic>CXCR3</topic><topic>Dermatitis - immunology</topic><topic>Hypersensitivity, Delayed - immunology</topic><topic>Immunologic Memory</topic><topic>Inflammation</topic><topic>Lymphocyte Activation</topic><topic>Mice</topic><topic>Receptors, Chemokine - analysis</topic><topic>Receptors, Chemokine - physiology</topic><topic>Receptors, CXCR3</topic><topic>Spleen - immunology</topic><topic>T cell</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mohan, Karkada</creatorcontrib><creatorcontrib>Cordeiro, Erin</creatorcontrib><creatorcontrib>Vaci, Maria</creatorcontrib><creatorcontrib>McMaster, Christopher</creatorcontrib><creatorcontrib>Issekutz, Thomas B.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>European journal of immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mohan, Karkada</au><au>Cordeiro, Erin</au><au>Vaci, Maria</au><au>McMaster, Christopher</au><au>Issekutz, Thomas B.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CXCR3 is required for migration to dermal inflammation by normal and in vivo activated T cells: differential requirements by CD4 and CD8 memory subsets</atitle><jtitle>European journal of immunology</jtitle><addtitle>Eur J Immunol</addtitle><date>2005-06</date><risdate>2005</risdate><volume>35</volume><issue>6</issue><spage>1702</spage><epage>1711</epage><pages>1702-1711</pages><issn>0014-2980</issn><eissn>1521-4141</eissn><abstract>Lymphocytes in inflamed tissues express numerous chemokine receptors. The relative importance of these receptors for migration in inflammation is unclear. The role of CXCR3 in T cell subset migration was examined using monoclonal antibodies developed to rat CXCR3. CXCR3 was expressed on sixfold more CD8+ (∼30%) than CD4+ (∼5%) T cells in spleen, lymph nodes and blood, and on ∼10% of CD4+CD45RC– (memory) and ∼50% of CD8+CD45RC+ spleen T cells. After immunization, CXCR3 increased tenfold on CD4+ lymph node lymphoblasts (∼55%), and >90% of inflammatory exudate T cells were CXCR3+. CXCR3+ T cells migrated significantly better than CXCR3– T cells to all dermal inflammatory stimuli tested in vivo, even though these T cells are a minority of the memory T cells. Blocking CXCR3 inhibited recruitment of 60–85% of unstimulated T cells and up to 90% of CD8+CD45RC+ effector T cells, but caused <50% inhibition of CD4+ and CD8+ memory (CD45RC–) T cells. About 90% of T lymphoblast migration to IFN‐γ, IFN‐γ plus TNF‐α, polyinosinic polycytidylic acid, lipopolysaccharide, and delayed‐type hypersensitivity (DTH)‐induced inflammation was inhibited. Blockade also reduced DTH‐induced induration. Thus, CXCR3 has a non‐redundant role in T cell migration to dermal inflammation and is critical for activated T lymphoblast recruitment, but memory T cells are less dependent on CXCR3 for their infiltration.</abstract><cop>Weinheim</cop><pub>WILEY‐VCH Verlag</pub><pmid>15884054</pmid><doi>10.1002/eji.200425885</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals CD4-Positive T-Lymphocytes - immunology CD8-Positive T-Lymphocytes - immunology Cell Adhesion Cell Movement Cell trafficking Chemokines Chemotaxis, Leukocyte CHO Cells Cricetinae CXCR3 Dermatitis - immunology Hypersensitivity, Delayed - immunology Immunologic Memory Inflammation Lymphocyte Activation Mice Receptors, Chemokine - analysis Receptors, Chemokine - physiology Receptors, CXCR3 Spleen - immunology T cell |
| title | CXCR3 is required for migration to dermal inflammation by normal and in vivo activated T cells: differential requirements by CD4 and CD8 memory subsets |
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