TGF-beta 2 decreases migration of lymphocytes in vitro and homing of cells into the central nervous system in vivo
Migration of leukocytes through an in vitro, cell culture model of the blood-brain barrier (BBB) composed of murine brain microvessel endothelial (En) cells and astrocytes, and in vivo in experimental allergic encephalomyelitis (EAE), was investigated. We have recently shown that the adhesiveness of...
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Veröffentlicht in: | The Journal of immunology (1950) 1995-07, Vol.155 (1), p.325-332 |
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creator | Fabry, Z Topham, DJ Fee, D Herlein, J Carlino, JA Hart, MN Sriram, S |
description | Migration of leukocytes through an in vitro, cell culture model of the blood-brain barrier (BBB) composed of murine brain microvessel endothelial (En) cells and astrocytes, and in vivo in experimental allergic encephalomyelitis (EAE), was investigated. We have recently shown that the adhesiveness of cultured murine brain microvascular endothelial cells for lymphocytes can be increased significantly by pretreatment with IL-1 beta, TNF-alpha, IFN-gamma, and LPS. In the present study, we investigated the role of TGF-beta 2 on the migration of leukocytes through the BBB. In vitro migration was assessed by measuring the percentage of 51Cr-labeled leukocytes migrating through the En/astrocyte monolayers. The basal level of migration was up-regulated significantly by treating the En/astrocyte monolayers with IL-1 alpha, IFN-gamma, TNF-alpha, and LPS. The ability of these cytokines to modulate migration was dose-dependent. Treatment of En cell/astrocyte monolayers with TGF-beta 2 down-regulated the level of leukocyte migration up-regulated by IL-1 alpha, IFN-gamma, and TNF-alpha in vitro in a dose-dependent manner. TGF-beta 2 also inhibited the migration of lymphocytes into the central nervous system (CNS) in vivo in a dose-dependent fashion. Taken together, these findings strongly suggest that TGF-beta plays an important role in the reduction of lymphocyte infiltration into the CNS in inflammatory demyelinating diseases such as EAE. |
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We have recently shown that the adhesiveness of cultured murine brain microvascular endothelial cells for lymphocytes can be increased significantly by pretreatment with IL-1 beta, TNF-alpha, IFN-gamma, and LPS. In the present study, we investigated the role of TGF-beta 2 on the migration of leukocytes through the BBB. In vitro migration was assessed by measuring the percentage of 51Cr-labeled leukocytes migrating through the En/astrocyte monolayers. The basal level of migration was up-regulated significantly by treating the En/astrocyte monolayers with IL-1 alpha, IFN-gamma, TNF-alpha, and LPS. The ability of these cytokines to modulate migration was dose-dependent. Treatment of En cell/astrocyte monolayers with TGF-beta 2 down-regulated the level of leukocyte migration up-regulated by IL-1 alpha, IFN-gamma, and TNF-alpha in vitro in a dose-dependent manner. TGF-beta 2 also inhibited the migration of lymphocytes into the central nervous system (CNS) in vivo in a dose-dependent fashion. Taken together, these findings strongly suggest that TGF-beta plays an important role in the reduction of lymphocyte infiltration into the CNS in inflammatory demyelinating diseases such as EAE.</description><identifier>ISSN: 0022-1767</identifier><identifier>EISSN: 1550-6606</identifier><identifier>DOI: 10.4049/jimmunol.155.1.325</identifier><identifier>PMID: 7602108</identifier><language>eng</language><publisher>United States: Am Assoc Immnol</publisher><subject>Animals ; Blood-Brain Barrier - drug effects ; Cell Adhesion - immunology ; Cell Movement - drug effects ; Cell Movement - physiology ; Cells, Cultured ; Central Nervous System - immunology ; Dose-Response Relationship, Immunologic ; Down-Regulation ; Encephalomyelitis, Autoimmune, Experimental - etiology ; Endothelium, Vascular - immunology ; Female ; Leukocytes - cytology ; Lymphocytes - cytology ; Mice ; Mice, Inbred Strains ; Receptors, Lymphocyte Homing - physiology ; Transforming Growth Factor beta - physiology</subject><ispartof>The Journal of immunology (1950), 1995-07, Vol.155 (1), p.325-332</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c336t-1835841b6211a41a99883553af84f8a936c04c9db631cda36ef01669806637193</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7602108$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fabry, Z</creatorcontrib><creatorcontrib>Topham, DJ</creatorcontrib><creatorcontrib>Fee, D</creatorcontrib><creatorcontrib>Herlein, J</creatorcontrib><creatorcontrib>Carlino, JA</creatorcontrib><creatorcontrib>Hart, MN</creatorcontrib><creatorcontrib>Sriram, S</creatorcontrib><title>TGF-beta 2 decreases migration of lymphocytes in vitro and homing of cells into the central nervous system in vivo</title><title>The Journal of immunology (1950)</title><addtitle>J Immunol</addtitle><description>Migration of leukocytes through an in vitro, cell culture model of the blood-brain barrier (BBB) composed of murine brain microvessel endothelial (En) cells and astrocytes, and in vivo in experimental allergic encephalomyelitis (EAE), was investigated. We have recently shown that the adhesiveness of cultured murine brain microvascular endothelial cells for lymphocytes can be increased significantly by pretreatment with IL-1 beta, TNF-alpha, IFN-gamma, and LPS. In the present study, we investigated the role of TGF-beta 2 on the migration of leukocytes through the BBB. In vitro migration was assessed by measuring the percentage of 51Cr-labeled leukocytes migrating through the En/astrocyte monolayers. The basal level of migration was up-regulated significantly by treating the En/astrocyte monolayers with IL-1 alpha, IFN-gamma, TNF-alpha, and LPS. The ability of these cytokines to modulate migration was dose-dependent. Treatment of En cell/astrocyte monolayers with TGF-beta 2 down-regulated the level of leukocyte migration up-regulated by IL-1 alpha, IFN-gamma, and TNF-alpha in vitro in a dose-dependent manner. TGF-beta 2 also inhibited the migration of lymphocytes into the central nervous system (CNS) in vivo in a dose-dependent fashion. Taken together, these findings strongly suggest that TGF-beta plays an important role in the reduction of lymphocyte infiltration into the CNS in inflammatory demyelinating diseases such as EAE.</description><subject>Animals</subject><subject>Blood-Brain Barrier - drug effects</subject><subject>Cell Adhesion - immunology</subject><subject>Cell Movement - drug effects</subject><subject>Cell Movement - physiology</subject><subject>Cells, Cultured</subject><subject>Central Nervous System - immunology</subject><subject>Dose-Response Relationship, Immunologic</subject><subject>Down-Regulation</subject><subject>Encephalomyelitis, Autoimmune, Experimental - etiology</subject><subject>Endothelium, Vascular - immunology</subject><subject>Female</subject><subject>Leukocytes - cytology</subject><subject>Lymphocytes - cytology</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Receptors, Lymphocyte Homing - physiology</subject><subject>Transforming Growth Factor beta - physiology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1995</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1OwzAQhC0EglJ4ASQkn7ileGPHiY8I8SdV4gJny02cxlUcF9tt1bfHUQscOe2ud2a80ofQDZAZI0zcr4y1m8H1MyiKGcxoXpygSepJxjnhp2hCSJ5nUPLyAl2GsCKEcJKzc3RepgqkmiD_8fKcLXRUOMeNrr1WQQdszdKraNyAXYv7vV13rt7HtDAD3proHVZDgztnzbAcJbXu-3EZHY6dTuMQverxoP3WbQIO-xC1PZi37gqdtaoP-vpYp-jz-enj8TWbv7-8PT7Ms5pSHjOoaFExWPAcQDFQQlTppaCqrVhbKUF5TVgtmgWnUDeKct0S4FxUhHNagqBTdHfIXXv3tdEhSmvCeKkadLpKliUVVDD2rxB4lRdj6hTlB2HtXQhet3LtjVV-L4HIkYj8ISITBQkyEUmm22P6ZmF182s5Ivj7vTPLbme8lsGqvk9qkLvd7i_oG6FXliU</recordid><startdate>19950701</startdate><enddate>19950701</enddate><creator>Fabry, Z</creator><creator>Topham, DJ</creator><creator>Fee, D</creator><creator>Herlein, J</creator><creator>Carlino, JA</creator><creator>Hart, MN</creator><creator>Sriram, S</creator><general>Am Assoc Immnol</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>7T5</scope><scope>H94</scope><scope>7X8</scope></search><sort><creationdate>19950701</creationdate><title>TGF-beta 2 decreases migration of lymphocytes in vitro and homing of cells into the central nervous system in vivo</title><author>Fabry, Z ; Topham, DJ ; Fee, D ; Herlein, J ; Carlino, JA ; Hart, MN ; Sriram, S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c336t-1835841b6211a41a99883553af84f8a936c04c9db631cda36ef01669806637193</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1995</creationdate><topic>Animals</topic><topic>Blood-Brain Barrier - drug effects</topic><topic>Cell Adhesion - immunology</topic><topic>Cell Movement - drug effects</topic><topic>Cell Movement - physiology</topic><topic>Cells, Cultured</topic><topic>Central Nervous System - immunology</topic><topic>Dose-Response Relationship, Immunologic</topic><topic>Down-Regulation</topic><topic>Encephalomyelitis, Autoimmune, Experimental - etiology</topic><topic>Endothelium, Vascular - immunology</topic><topic>Female</topic><topic>Leukocytes - cytology</topic><topic>Lymphocytes - cytology</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Receptors, Lymphocyte Homing - physiology</topic><topic>Transforming Growth Factor beta - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fabry, Z</creatorcontrib><creatorcontrib>Topham, DJ</creatorcontrib><creatorcontrib>Fee, D</creatorcontrib><creatorcontrib>Herlein, J</creatorcontrib><creatorcontrib>Carlino, JA</creatorcontrib><creatorcontrib>Hart, MN</creatorcontrib><creatorcontrib>Sriram, S</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fabry, Z</au><au>Topham, DJ</au><au>Fee, D</au><au>Herlein, J</au><au>Carlino, JA</au><au>Hart, MN</au><au>Sriram, S</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>TGF-beta 2 decreases migration of lymphocytes in vitro and homing of cells into the central nervous system in vivo</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>1995-07-01</date><risdate>1995</risdate><volume>155</volume><issue>1</issue><spage>325</spage><epage>332</epage><pages>325-332</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Migration of leukocytes through an in vitro, cell culture model of the blood-brain barrier (BBB) composed of murine brain microvessel endothelial (En) cells and astrocytes, and in vivo in experimental allergic encephalomyelitis (EAE), was investigated. We have recently shown that the adhesiveness of cultured murine brain microvascular endothelial cells for lymphocytes can be increased significantly by pretreatment with IL-1 beta, TNF-alpha, IFN-gamma, and LPS. In the present study, we investigated the role of TGF-beta 2 on the migration of leukocytes through the BBB. In vitro migration was assessed by measuring the percentage of 51Cr-labeled leukocytes migrating through the En/astrocyte monolayers. The basal level of migration was up-regulated significantly by treating the En/astrocyte monolayers with IL-1 alpha, IFN-gamma, TNF-alpha, and LPS. The ability of these cytokines to modulate migration was dose-dependent. Treatment of En cell/astrocyte monolayers with TGF-beta 2 down-regulated the level of leukocyte migration up-regulated by IL-1 alpha, IFN-gamma, and TNF-alpha in vitro in a dose-dependent manner. TGF-beta 2 also inhibited the migration of lymphocytes into the central nervous system (CNS) in vivo in a dose-dependent fashion. Taken together, these findings strongly suggest that TGF-beta plays an important role in the reduction of lymphocyte infiltration into the CNS in inflammatory demyelinating diseases such as EAE.</abstract><cop>United States</cop><pub>Am Assoc Immnol</pub><pmid>7602108</pmid><doi>10.4049/jimmunol.155.1.325</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Blood-Brain Barrier - drug effects Cell Adhesion - immunology Cell Movement - drug effects Cell Movement - physiology Cells, Cultured Central Nervous System - immunology Dose-Response Relationship, Immunologic Down-Regulation Encephalomyelitis, Autoimmune, Experimental - etiology Endothelium, Vascular - immunology Female Leukocytes - cytology Lymphocytes - cytology Mice Mice, Inbred Strains Receptors, Lymphocyte Homing - physiology Transforming Growth Factor beta - physiology |
title | TGF-beta 2 decreases migration of lymphocytes in vitro and homing of cells into the central nervous system in vivo |
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