Loading…

Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis

After primary immunization with myelin/oligodendrocyte glycoprotein, CD28−/− mice developed experimental autoimmune meningitis (EAM) rather than experimental autoimmune encephalomyelitis (EAE). Cytokine and chemokine production in EAE and EAM were compared to understand the differences in disease ph...

Full description

Saved in:
Bibliographic Details
Published in:Clinical immunology (Orlando, Fla.) Fla.), 2000-02, Vol.94 (2), p.114-124
Main Authors: Perrin, Peter J., Rumbley, Catherine A., Beswick, Richard L., Lavi, Ehud, Phillips, S.Michael
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
cited_by cdi_FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13
cites cdi_FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13
container_end_page 124
container_issue 2
container_start_page 114
container_title Clinical immunology (Orlando, Fla.)
container_volume 94
creator Perrin, Peter J.
Rumbley, Catherine A.
Beswick, Richard L.
Lavi, Ehud
Phillips, S.Michael
description After primary immunization with myelin/oligodendrocyte glycoprotein, CD28−/− mice developed experimental autoimmune meningitis (EAM) rather than experimental autoimmune encephalomyelitis (EAE). Cytokine and chemokine production in EAE and EAM were compared to understand the differences in disease phenotype. T cells from the central nervous system lesions of mice with either EAE or EAM expressed intracellular TNF-α. Splenic T cells from mice with EAM produced TNF-α and IL-6 but no IL-2. Conversely, EAE-derived splenic T cells produced TNF-α and IL-2 but no IL-6. Altered T cell differentiation in EAM was not due to a Th1 to Th2 shift, because equivalent amounts of T cell IFN-γ mRNA were produced in both diseases. Neutrophils also produced inflammatory mediators such as TNF-α and IL-6 in EAM. Autocrine production of MIP-2 mRNA was observed in neutrophils from mice with EAM but not EAE. Therefore, distinct patterns of cytokines and chemokines distinguish EAE and EAM.
doi_str_mv 10.1006/clim.1999.4825
format article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_70869340</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S1521661699948258</els_id><sourcerecordid>17508673</sourcerecordid><originalsourceid>FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13</originalsourceid><addsrcrecordid>eNqFkUFv3CAQhVHVqEnTXnOM9lD1thvABswx2mzTSqmSw94RhnFDa8MGcJTtf-h_Dq5XSi9RTzODvvc0zEPojOAVwZhfmN4NKyKlXNUNZW_QCWGULAWu2NtDzznhx-h9Sj8xxoxS_g4dE8wrgSU_QX-uXNdBBJ-d7hfrfQ6_nIeF9naxvodhnu5isKPJLvjyqKM2GaL7DWmxedqVbijqIr4cc3DDMBbBd_DO_3DZpb9Or2Ebb2B3r_sw7KGf6A_oqNN9go-Heoq2Xzbb9dflze31t_XlzdLUGOelrXHLQEtBrBUWVw1tREdZ23JWW6mpEJJBSyvCOoZbYMKANbxrG0Fk3ZLqFH2ebXcxPIyQshpcMtD32kMYkxK44bKq8X9BIlhBRVXA1QyaGFKK0Kld-bCOe0WwmoJSU1BqCkpNQRXB-cF5bAew_-BzMgX4dAB0MrrvovbGpReuEpQTWbBmxqCc69FBVMk4KHe1LoLJygb32grPYTKy4Q</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>17508673</pqid></control><display><type>article</type><title>Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis</title><source>ScienceDirect Freedom Collection</source><creator>Perrin, Peter J. ; Rumbley, Catherine A. ; Beswick, Richard L. ; Lavi, Ehud ; Phillips, S.Michael</creator><creatorcontrib>Perrin, Peter J. ; Rumbley, Catherine A. ; Beswick, Richard L. ; Lavi, Ehud ; Phillips, S.Michael</creatorcontrib><description>After primary immunization with myelin/oligodendrocyte glycoprotein, CD28−/− mice developed experimental autoimmune meningitis (EAM) rather than experimental autoimmune encephalomyelitis (EAE). Cytokine and chemokine production in EAE and EAM were compared to understand the differences in disease phenotype. T cells from the central nervous system lesions of mice with either EAE or EAM expressed intracellular TNF-α. Splenic T cells from mice with EAM produced TNF-α and IL-6 but no IL-2. Conversely, EAE-derived splenic T cells produced TNF-α and IL-2 but no IL-6. Altered T cell differentiation in EAM was not due to a Th1 to Th2 shift, because equivalent amounts of T cell IFN-γ mRNA were produced in both diseases. Neutrophils also produced inflammatory mediators such as TNF-α and IL-6 in EAM. Autocrine production of MIP-2 mRNA was observed in neutrophils from mice with EAM but not EAE. Therefore, distinct patterns of cytokines and chemokines distinguish EAE and EAM.</description><identifier>ISSN: 1521-6616</identifier><identifier>EISSN: 1521-7035</identifier><identifier>DOI: 10.1006/clim.1999.4825</identifier><identifier>PMID: 10637096</identifier><identifier>CODEN: CLIIFY</identifier><language>eng</language><publisher>San Diego, CA: Elsevier Inc</publisher><subject>AIDS/HIV ; Amino Acid Sequence ; Animals ; Autoimmune Diseases - immunology ; Autoimmune Diseases - pathology ; Biological and medical sciences ; Brain - pathology ; CD28 ; CD28 antigen ; Chemokines - biosynthesis ; Cytokines - biosynthesis ; Disease Models, Animal ; encephalomyelitis ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Experimental and animal immunopathology. Animal models ; IL-2 ; IL-6 ; Immunopathology ; Lymphocyte Activation ; Medical sciences ; meningitis ; Meningitis - immunology ; Meningitis - pathology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis ; Neurology ; Receptors, Chemokine - metabolism ; Spleen - cytology ; Spleen - immunology ; T-Lymphocytes - immunology ; Th1 Cells - immunology ; Th2 Cells - immunology</subject><ispartof>Clinical immunology (Orlando, Fla.), 2000-02, Vol.94 (2), p.114-124</ispartof><rights>2000 Academic Press</rights><rights>2000 INIST-CNRS</rights><rights>Copyright 2000 Academic Press.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13</citedby><cites>FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=1372619$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10637096$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Perrin, Peter J.</creatorcontrib><creatorcontrib>Rumbley, Catherine A.</creatorcontrib><creatorcontrib>Beswick, Richard L.</creatorcontrib><creatorcontrib>Lavi, Ehud</creatorcontrib><creatorcontrib>Phillips, S.Michael</creatorcontrib><title>Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis</title><title>Clinical immunology (Orlando, Fla.)</title><addtitle>Clin Immunol</addtitle><description>After primary immunization with myelin/oligodendrocyte glycoprotein, CD28−/− mice developed experimental autoimmune meningitis (EAM) rather than experimental autoimmune encephalomyelitis (EAE). Cytokine and chemokine production in EAE and EAM were compared to understand the differences in disease phenotype. T cells from the central nervous system lesions of mice with either EAE or EAM expressed intracellular TNF-α. Splenic T cells from mice with EAM produced TNF-α and IL-6 but no IL-2. Conversely, EAE-derived splenic T cells produced TNF-α and IL-2 but no IL-6. Altered T cell differentiation in EAM was not due to a Th1 to Th2 shift, because equivalent amounts of T cell IFN-γ mRNA were produced in both diseases. Neutrophils also produced inflammatory mediators such as TNF-α and IL-6 in EAM. Autocrine production of MIP-2 mRNA was observed in neutrophils from mice with EAM but not EAE. Therefore, distinct patterns of cytokines and chemokines distinguish EAE and EAM.</description><subject>AIDS/HIV</subject><subject>Amino Acid Sequence</subject><subject>Animals</subject><subject>Autoimmune Diseases - immunology</subject><subject>Autoimmune Diseases - pathology</subject><subject>Biological and medical sciences</subject><subject>Brain - pathology</subject><subject>CD28</subject><subject>CD28 antigen</subject><subject>Chemokines - biosynthesis</subject><subject>Cytokines - biosynthesis</subject><subject>Disease Models, Animal</subject><subject>encephalomyelitis</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Experimental and animal immunopathology. Animal models</subject><subject>IL-2</subject><subject>IL-6</subject><subject>Immunopathology</subject><subject>Lymphocyte Activation</subject><subject>Medical sciences</subject><subject>meningitis</subject><subject>Meningitis - immunology</subject><subject>Meningitis - pathology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Molecular Sequence Data</subject><subject>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</subject><subject>Neurology</subject><subject>Receptors, Chemokine - metabolism</subject><subject>Spleen - cytology</subject><subject>Spleen - immunology</subject><subject>T-Lymphocytes - immunology</subject><subject>Th1 Cells - immunology</subject><subject>Th2 Cells - immunology</subject><issn>1521-6616</issn><issn>1521-7035</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNqFkUFv3CAQhVHVqEnTXnOM9lD1thvABswx2mzTSqmSw94RhnFDa8MGcJTtf-h_Dq5XSi9RTzODvvc0zEPojOAVwZhfmN4NKyKlXNUNZW_QCWGULAWu2NtDzznhx-h9Sj8xxoxS_g4dE8wrgSU_QX-uXNdBBJ-d7hfrfQ6_nIeF9naxvodhnu5isKPJLvjyqKM2GaL7DWmxedqVbijqIr4cc3DDMBbBd_DO_3DZpb9Or2Ebb2B3r_sw7KGf6A_oqNN9go-Heoq2Xzbb9dflze31t_XlzdLUGOelrXHLQEtBrBUWVw1tREdZ23JWW6mpEJJBSyvCOoZbYMKANbxrG0Fk3ZLqFH2ebXcxPIyQshpcMtD32kMYkxK44bKq8X9BIlhBRVXA1QyaGFKK0Kld-bCOe0WwmoJSU1BqCkpNQRXB-cF5bAew_-BzMgX4dAB0MrrvovbGpReuEpQTWbBmxqCc69FBVMk4KHe1LoLJygb32grPYTKy4Q</recordid><startdate>20000201</startdate><enddate>20000201</enddate><creator>Perrin, Peter J.</creator><creator>Rumbley, Catherine A.</creator><creator>Beswick, Richard L.</creator><creator>Lavi, Ehud</creator><creator>Phillips, S.Michael</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>IQODW</scope><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>20000201</creationdate><title>Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis</title><author>Perrin, Peter J. ; Rumbley, Catherine A. ; Beswick, Richard L. ; Lavi, Ehud ; Phillips, S.Michael</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>AIDS/HIV</topic><topic>Amino Acid Sequence</topic><topic>Animals</topic><topic>Autoimmune Diseases - immunology</topic><topic>Autoimmune Diseases - pathology</topic><topic>Biological and medical sciences</topic><topic>Brain - pathology</topic><topic>CD28</topic><topic>CD28 antigen</topic><topic>Chemokines - biosynthesis</topic><topic>Cytokines - biosynthesis</topic><topic>Disease Models, Animal</topic><topic>encephalomyelitis</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Experimental and animal immunopathology. Animal models</topic><topic>IL-2</topic><topic>IL-6</topic><topic>Immunopathology</topic><topic>Lymphocyte Activation</topic><topic>Medical sciences</topic><topic>meningitis</topic><topic>Meningitis - immunology</topic><topic>Meningitis - pathology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Molecular Sequence Data</topic><topic>Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis</topic><topic>Neurology</topic><topic>Receptors, Chemokine - metabolism</topic><topic>Spleen - cytology</topic><topic>Spleen - immunology</topic><topic>T-Lymphocytes - immunology</topic><topic>Th1 Cells - immunology</topic><topic>Th2 Cells - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Perrin, Peter J.</creatorcontrib><creatorcontrib>Rumbley, Catherine A.</creatorcontrib><creatorcontrib>Beswick, Richard L.</creatorcontrib><creatorcontrib>Lavi, Ehud</creatorcontrib><creatorcontrib>Phillips, S.Michael</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>CrossRef</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Clinical immunology (Orlando, Fla.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Perrin, Peter J.</au><au>Rumbley, Catherine A.</au><au>Beswick, Richard L.</au><au>Lavi, Ehud</au><au>Phillips, S.Michael</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis</atitle><jtitle>Clinical immunology (Orlando, Fla.)</jtitle><addtitle>Clin Immunol</addtitle><date>2000-02-01</date><risdate>2000</risdate><volume>94</volume><issue>2</issue><spage>114</spage><epage>124</epage><pages>114-124</pages><issn>1521-6616</issn><eissn>1521-7035</eissn><coden>CLIIFY</coden><abstract>After primary immunization with myelin/oligodendrocyte glycoprotein, CD28−/− mice developed experimental autoimmune meningitis (EAM) rather than experimental autoimmune encephalomyelitis (EAE). Cytokine and chemokine production in EAE and EAM were compared to understand the differences in disease phenotype. T cells from the central nervous system lesions of mice with either EAE or EAM expressed intracellular TNF-α. Splenic T cells from mice with EAM produced TNF-α and IL-6 but no IL-2. Conversely, EAE-derived splenic T cells produced TNF-α and IL-2 but no IL-6. Altered T cell differentiation in EAM was not due to a Th1 to Th2 shift, because equivalent amounts of T cell IFN-γ mRNA were produced in both diseases. Neutrophils also produced inflammatory mediators such as TNF-α and IL-6 in EAM. Autocrine production of MIP-2 mRNA was observed in neutrophils from mice with EAM but not EAE. Therefore, distinct patterns of cytokines and chemokines distinguish EAE and EAM.</abstract><cop>San Diego, CA</cop><pub>Elsevier Inc</pub><pmid>10637096</pmid><doi>10.1006/clim.1999.4825</doi><tpages>11</tpages></addata></record>
fulltext fulltext
identifier ISSN: 1521-6616
ispartof Clinical immunology (Orlando, Fla.), 2000-02, Vol.94 (2), p.114-124
issn 1521-6616
1521-7035
language eng
recordid cdi_proquest_miscellaneous_70869340
source ScienceDirect Freedom Collection
subjects AIDS/HIV
Amino Acid Sequence
Animals
Autoimmune Diseases - immunology
Autoimmune Diseases - pathology
Biological and medical sciences
Brain - pathology
CD28
CD28 antigen
Chemokines - biosynthesis
Cytokines - biosynthesis
Disease Models, Animal
encephalomyelitis
Encephalomyelitis, Autoimmune, Experimental - immunology
Encephalomyelitis, Autoimmune, Experimental - pathology
Experimental and animal immunopathology. Animal models
IL-2
IL-6
Immunopathology
Lymphocyte Activation
Medical sciences
meningitis
Meningitis - immunology
Meningitis - pathology
Mice
Mice, Inbred C57BL
Molecular Sequence Data
Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis
Neurology
Receptors, Chemokine - metabolism
Spleen - cytology
Spleen - immunology
T-Lymphocytes - immunology
Th1 Cells - immunology
Th2 Cells - immunology
title Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis
url http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-25T13%3A10%3A37IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Differential%20Cytokine%20and%20Chemokine%20Production%20Characterizes%20Experimental%20Autoimmune%20Meningitis%20and%20Experimental%20Autoimmune%20Encephalomyelitis&rft.jtitle=Clinical%20immunology%20(Orlando,%20Fla.)&rft.au=Perrin,%20Peter%20J.&rft.date=2000-02-01&rft.volume=94&rft.issue=2&rft.spage=114&rft.epage=124&rft.pages=114-124&rft.issn=1521-6616&rft.eissn=1521-7035&rft.coden=CLIIFY&rft_id=info:doi/10.1006/clim.1999.4825&rft_dat=%3Cproquest_cross%3E17508673%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c400t-d40b5ea971dd7d038287f25bb654d9a27795eb2315f50be57cedc6fb87194b13%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=17508673&rft_id=info:pmid/10637096&rfr_iscdi=true