T-Cell Apoptosis in Inflammatory Brain Lesions : Destruction of T Cells Does Not Depend on Antigen Recognition
Elimination of inflammatory T cells by apoptosis appears to play an important role in the down-regulation of inflammation in the central nervous system. Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of autoimmune encephalomyelitis. Apoptosis is restric...
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| Veröffentlicht in: | The American journal of pathology 1998-09, Vol.153 (3), p.715-724 |
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| container_title | The American journal of pathology |
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| creator | Bauer, Jan Bradl, Monika Hickey, William F Forss-Petter, Sonja Breitschopf, Helene Linington, Chris Wekerle, Hartmut Lassmann, Hans |
| description | Elimination of inflammatory T cells by apoptosis appears to play an important role in the down-regulation of inflammation in the central nervous system. Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of autoimmune encephalomyelitis. Apoptosis is restricted to cells located in the neuroectodermal parenchyma, thereby leaving T cells present in the brain's connective tissue compartments unharmed. Death of T cells in the parenchyma does not depend on antigen presentation by resident microglial cells or astrocytes. Adoptive transfer experiments with T lymphocytes carrying a specific genetic marker revealed that in the central nervous system these cells are destroyed regardless of their antigen specificity or state of activation. Although many of both antigen-dependent and -independent mechanisms in the induction of T-cell apoptosis may act simultaneously, our results suggest that the nervous system harbors a specific, currently undefined, mechanism that effectively eliminates infiltrating T lymphocytes. |
| doi_str_mv | 10.1016/S0002-9440(10)65615-5 |
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Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of autoimmune encephalomyelitis. Apoptosis is restricted to cells located in the neuroectodermal parenchyma, thereby leaving T cells present in the brain's connective tissue compartments unharmed. Death of T cells in the parenchyma does not depend on antigen presentation by resident microglial cells or astrocytes. Adoptive transfer experiments with T lymphocytes carrying a specific genetic marker revealed that in the central nervous system these cells are destroyed regardless of their antigen specificity or state of activation. Although many of both antigen-dependent and -independent mechanisms in the induction of T-cell apoptosis may act simultaneously, our results suggest that the nervous system harbors a specific, currently undefined, mechanism that effectively eliminates infiltrating T lymphocytes.</description><identifier>ISSN: 0002-9440</identifier><identifier>EISSN: 1525-2191</identifier><identifier>DOI: 10.1016/S0002-9440(10)65615-5</identifier><identifier>PMID: 9736022</identifier><identifier>CODEN: AJPAA4</identifier><language>eng</language><publisher>Bethesda, MD: ASIP</publisher><subject>Animals ; Animals, Genetically Modified ; Antigen Presentation - immunology ; Apoptosis - immunology ; Biological and medical sciences ; Brain - immunology ; Brain - pathology ; Cell Count ; Cell Death ; Cell Movement - immunology ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Immunoenzyme Techniques ; Medical sciences ; Myelin Basic Protein - immunology ; Nervous system involvement in other diseases. Miscellaneous ; Neurology ; Rats ; Rats, Inbred Lew ; Regular ; Spinal Cord - immunology ; Spinal Cord - pathology ; T-Lymphocytes - immunology ; T-Lymphocytes - pathology</subject><ispartof>The American journal of pathology, 1998-09, Vol.153 (3), p.715-724</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Society for Investigative Pathology Sep 1998</rights><rights>Copyright © 1998, American Society for Investigative Pathology</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1853020/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1853020/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,727,780,784,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2386815$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9736022$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bauer, Jan</creatorcontrib><creatorcontrib>Bradl, Monika</creatorcontrib><creatorcontrib>Hickey, William F</creatorcontrib><creatorcontrib>Forss-Petter, Sonja</creatorcontrib><creatorcontrib>Breitschopf, Helene</creatorcontrib><creatorcontrib>Linington, Chris</creatorcontrib><creatorcontrib>Wekerle, Hartmut</creatorcontrib><creatorcontrib>Lassmann, Hans</creatorcontrib><title>T-Cell Apoptosis in Inflammatory Brain Lesions : Destruction of T Cells Does Not Depend on Antigen Recognition</title><title>The American journal of pathology</title><addtitle>Am J Pathol</addtitle><description>Elimination of inflammatory T cells by apoptosis appears to play an important role in the down-regulation of inflammation in the central nervous system. Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of autoimmune encephalomyelitis. Apoptosis is restricted to cells located in the neuroectodermal parenchyma, thereby leaving T cells present in the brain's connective tissue compartments unharmed. Death of T cells in the parenchyma does not depend on antigen presentation by resident microglial cells or astrocytes. Adoptive transfer experiments with T lymphocytes carrying a specific genetic marker revealed that in the central nervous system these cells are destroyed regardless of their antigen specificity or state of activation. Although many of both antigen-dependent and -independent mechanisms in the induction of T-cell apoptosis may act simultaneously, our results suggest that the nervous system harbors a specific, currently undefined, mechanism that effectively eliminates infiltrating T lymphocytes.</description><subject>Animals</subject><subject>Animals, Genetically Modified</subject><subject>Antigen Presentation - immunology</subject><subject>Apoptosis - immunology</subject><subject>Biological and medical sciences</subject><subject>Brain - immunology</subject><subject>Brain - pathology</subject><subject>Cell Count</subject><subject>Cell Death</subject><subject>Cell Movement - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Immunoenzyme Techniques</subject><subject>Medical sciences</subject><subject>Myelin Basic Protein - immunology</subject><subject>Nervous system involvement in other diseases. Miscellaneous</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Regular</subject><subject>Spinal Cord - immunology</subject><subject>Spinal Cord - pathology</subject><subject>T-Lymphocytes - immunology</subject><subject>T-Lymphocytes - pathology</subject><issn>0002-9440</issn><issn>1525-2191</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1998</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><recordid>eNpdUduKFDEUDOKyjqufsBBERB9ac-1O9kEYZ90LDAo6Pod0OpnJ0J20Sbeyf28Gh_HyVJxUnTpVBIBLjN5ihOt3XxFCpJKModcYval5jXnFH4EF5oRXBEv8GCxOkifgac77MtZUoHNwLhtaI0IWIGyqle17uBzjOMXsM_QB3gfX62HQU0wP8EPS5Wlts48hwyt4bfOUZjOVEUYHN_Cwn-F1tBl-ilPhRxs6WNhlmPzWBvjFmrgN_rDxDJw53Wf7_IgX4NvNx83qrlp_vr1fLdfVjjIxVdoxbjosHGsE0R1DrXUt1kTWhGLputYxh1rNuMCokdgdkElLJLKtEcbQC_D-t-84t4PtjA1T0r0akx90elBRe_UvE_xObeMPhQWniKBi8OpokOL3uVRWg8-mNNXBxjmrhspymrMifPGfcB_nFEo5RbCQnNLm4Hb5d5xTjuM3FP7lkdfZ6N4lHYzPJxmhohaY_wm189vdT5-syoPu-2KKld6PRaGoagr8AkOZpOQ</recordid><startdate>19980901</startdate><enddate>19980901</enddate><creator>Bauer, Jan</creator><creator>Bradl, Monika</creator><creator>Hickey, William F</creator><creator>Forss-Petter, Sonja</creator><creator>Breitschopf, Helene</creator><creator>Linington, Chris</creator><creator>Wekerle, Hartmut</creator><creator>Lassmann, Hans</creator><general>ASIP</general><general>American Society for Investigative Pathology</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</scope><scope>8AF</scope><scope>8C1</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>19980901</creationdate><title>T-Cell Apoptosis in Inflammatory Brain Lesions : Destruction of T Cells Does Not Depend on Antigen Recognition</title><author>Bauer, Jan ; Bradl, Monika ; Hickey, William F ; Forss-Petter, Sonja ; Breitschopf, Helene ; Linington, Chris ; Wekerle, Hartmut ; Lassmann, Hans</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-h348t-af45cd18f4782ad40befb1a2962319fdbf4f0ba45810791f581049e290ebc8cc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Animals</topic><topic>Animals, Genetically Modified</topic><topic>Antigen Presentation - immunology</topic><topic>Apoptosis - immunology</topic><topic>Biological and medical sciences</topic><topic>Brain - immunology</topic><topic>Brain - pathology</topic><topic>Cell Count</topic><topic>Cell Death</topic><topic>Cell Movement - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Immunoenzyme Techniques</topic><topic>Medical sciences</topic><topic>Myelin Basic Protein - immunology</topic><topic>Nervous system involvement in other diseases. Miscellaneous</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Regular</topic><topic>Spinal Cord - immunology</topic><topic>Spinal Cord - pathology</topic><topic>T-Lymphocytes - immunology</topic><topic>T-Lymphocytes - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bauer, Jan</creatorcontrib><creatorcontrib>Bradl, Monika</creatorcontrib><creatorcontrib>Hickey, William F</creatorcontrib><creatorcontrib>Forss-Petter, Sonja</creatorcontrib><creatorcontrib>Breitschopf, Helene</creatorcontrib><creatorcontrib>Linington, Chris</creatorcontrib><creatorcontrib>Wekerle, Hartmut</creatorcontrib><creatorcontrib>Lassmann, Hans</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>STEM Database</collection><collection>Public Health Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>The American journal of pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bauer, Jan</au><au>Bradl, Monika</au><au>Hickey, William F</au><au>Forss-Petter, Sonja</au><au>Breitschopf, Helene</au><au>Linington, Chris</au><au>Wekerle, Hartmut</au><au>Lassmann, Hans</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>T-Cell Apoptosis in Inflammatory Brain Lesions : Destruction of T Cells Does Not Depend on Antigen Recognition</atitle><jtitle>The American journal of pathology</jtitle><addtitle>Am J Pathol</addtitle><date>1998-09-01</date><risdate>1998</risdate><volume>153</volume><issue>3</issue><spage>715</spage><epage>724</epage><pages>715-724</pages><issn>0002-9440</issn><eissn>1525-2191</eissn><coden>AJPAA4</coden><abstract>Elimination of inflammatory T cells by apoptosis appears to play an important role in the down-regulation of inflammation in the central nervous system. Here we report that apoptosis of T lymphocytes occurs to a similar extent in different models of autoimmune encephalomyelitis. Apoptosis is restricted to cells located in the neuroectodermal parenchyma, thereby leaving T cells present in the brain's connective tissue compartments unharmed. Death of T cells in the parenchyma does not depend on antigen presentation by resident microglial cells or astrocytes. Adoptive transfer experiments with T lymphocytes carrying a specific genetic marker revealed that in the central nervous system these cells are destroyed regardless of their antigen specificity or state of activation. Although many of both antigen-dependent and -independent mechanisms in the induction of T-cell apoptosis may act simultaneously, our results suggest that the nervous system harbors a specific, currently undefined, mechanism that effectively eliminates infiltrating T lymphocytes.</abstract><cop>Bethesda, MD</cop><pub>ASIP</pub><pmid>9736022</pmid><doi>10.1016/S0002-9440(10)65615-5</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Animals, Genetically Modified Antigen Presentation - immunology Apoptosis - immunology Biological and medical sciences Brain - immunology Brain - pathology Cell Count Cell Death Cell Movement - immunology Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - pathology Immunoenzyme Techniques Medical sciences Myelin Basic Protein - immunology Nervous system involvement in other diseases. Miscellaneous Neurology Rats Rats, Inbred Lew Regular Spinal Cord - immunology Spinal Cord - pathology T-Lymphocytes - immunology T-Lymphocytes - pathology |
| title | T-Cell Apoptosis in Inflammatory Brain Lesions : Destruction of T Cells Does Not Depend on Antigen Recognition |
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