GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage
Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS). MS lesions harbor different immune cells, but the contribution of individual cell types to disease etiology and progression is not well understood. In experimental autoimmune encephalomyelitis (EAE)...
Gespeichert in:
| Veröffentlicht in: | Trends in immunology 2015-10, Vol.36 (10), p.651-662 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 662 |
|---|---|
| container_issue | 10 |
| container_start_page | 651 |
| container_title | Trends in immunology |
| container_volume | 36 |
| creator | Croxford, Andrew L Spath, Sabine Becher, Burkhard |
| description | Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS). MS lesions harbor different immune cells, but the contribution of individual cell types to disease etiology and progression is not well understood. In experimental autoimmune encephalomyelitis (EAE), auto-reactive helper T (Th) cells instigate CNS inflammation by acting on myeloid cells via the production of granulocyte-macrophage colony-stimulating factor (GM-CSF). Recent reports have implicated myeloid cells in both the inflammatory process and as executers of tissue damage in the CNS. We review these findings here, and integrate them into a model wherein GM-CSF produced by Th cells coordinates monocyte recruitment to the CNS, and differentiation into pathogenic effectors. We discuss the implications of this model to current therapies for MS, and outline important areas of further inquiry. |
| doi_str_mv | 10.1016/j.it.2015.08.004 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1718912953</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>1_s2_0_S1471490615001969</els_id><sourcerecordid>3824688561</sourcerecordid><originalsourceid>FETCH-LOGICAL-c433t-b98b015ea4e63a58f3a19f365f07420c1ddb613895c3aecaac67971024278d333</originalsourceid><addsrcrecordid>eNp9kU1P3DAYhC1UVCj0zqmK1AuXBH8ltjkgoW2XVlrgAD1bXucN8jaxwU6Q9t_X6VIqceDk9_DMaDyD0AnBFcGkOdtUbqwoJnWFZYUx30OHhAtSciXJh9cbNwfoU0obnEEhxEd0QBvOiOL0EC2vrsvF3bJwvriBKQbnu94Mgxld8OfFylnwyfmH4noLfXBtsYC-T0UXYnHvUpqg-GYG8wDHaL8zfYLPL-8R-rX8fr_4Ua5ur34uLlel5YyN5VrJdQ4BhkPDTC07ZojqWFN3WHCKLWnbdUOYVLVlBqwxthFKEEw5FbJljB2h053vYwxPE6RRDy7ZnMl4CFPSRBCpCFX1jH59g27CFH1O95digjImM4V3lI0hpQidfoxuMHGrCdZzx3qj3ajnjjWWOnecJV9ejKf1AO2r4F-pGTjfAZCbeHYQdbIOvIXWRbCjboN7z_3ijdj2zjtr-t-whfT_DzpRjfXdvPE8ManzvKpR7A8s6p1e</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1718372338</pqid></control><display><type>article</type><title>GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage</title><source>MEDLINE</source><source>Elsevier ScienceDirect Journals</source><creator>Croxford, Andrew L ; Spath, Sabine ; Becher, Burkhard</creator><creatorcontrib>Croxford, Andrew L ; Spath, Sabine ; Becher, Burkhard</creatorcontrib><description>Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS). MS lesions harbor different immune cells, but the contribution of individual cell types to disease etiology and progression is not well understood. In experimental autoimmune encephalomyelitis (EAE), auto-reactive helper T (Th) cells instigate CNS inflammation by acting on myeloid cells via the production of granulocyte-macrophage colony-stimulating factor (GM-CSF). Recent reports have implicated myeloid cells in both the inflammatory process and as executers of tissue damage in the CNS. We review these findings here, and integrate them into a model wherein GM-CSF produced by Th cells coordinates monocyte recruitment to the CNS, and differentiation into pathogenic effectors. We discuss the implications of this model to current therapies for MS, and outline important areas of further inquiry.</description><identifier>ISSN: 1471-4906</identifier><identifier>EISSN: 1471-4981</identifier><identifier>DOI: 10.1016/j.it.2015.08.004</identifier><identifier>PMID: 26431942</identifier><language>eng</language><publisher>England: Elsevier Ltd</publisher><subject>Allergy and Immunology ; Animals ; Antigens ; Cell Communication ; Cell Differentiation ; Central Nervous System Diseases - genetics ; Central Nervous System Diseases - immunology ; Central Nervous System Diseases - metabolism ; Central Nervous System Diseases - pathology ; CNS ; Cytokines ; Disease ; Encephalomyelitis, Autoimmune, Experimental - genetics ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - metabolism ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Gene expression ; Gene Expression Regulation ; GM-CSF ; Granulocyte-Macrophage Colony-Stimulating Factor - genetics ; Granulocyte-Macrophage Colony-Stimulating Factor - metabolism ; Humans ; Inflammation ; Inflammation - genetics ; Inflammation - immunology ; Inflammation - metabolism ; Inflammation - pathology ; Lymphocytes ; monocytes ; Multiple Sclerosis - genetics ; Multiple Sclerosis - immunology ; Multiple Sclerosis - metabolism ; Multiple Sclerosis - pathology ; Multiple Sclerosis - therapy ; Myeloid Cells - cytology ; Myeloid Cells - immunology ; Myeloid Cells - metabolism ; Neuroimmunomodulation ; neuroinflammation ; Studies ; T-Lymphocytes, Helper-Inducer - immunology ; T-Lymphocytes, Helper-Inducer - metabolism ; Target recognition ; tissue damage ; Transcription factors</subject><ispartof>Trends in immunology, 2015-10, Vol.36 (10), p.651-662</ispartof><rights>Elsevier Ltd</rights><rights>2015 Elsevier Ltd</rights><rights>Copyright © 2015 Elsevier Ltd. All rights reserved.</rights><rights>Copyright Elsevier Limited Oct 2015</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c433t-b98b015ea4e63a58f3a19f365f07420c1ddb613895c3aecaac67971024278d333</citedby><cites>FETCH-LOGICAL-c433t-b98b015ea4e63a58f3a19f365f07420c1ddb613895c3aecaac67971024278d333</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S1471490615001969$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26431942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Croxford, Andrew L</creatorcontrib><creatorcontrib>Spath, Sabine</creatorcontrib><creatorcontrib>Becher, Burkhard</creatorcontrib><title>GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage</title><title>Trends in immunology</title><addtitle>Trends Immunol</addtitle><description>Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS). MS lesions harbor different immune cells, but the contribution of individual cell types to disease etiology and progression is not well understood. In experimental autoimmune encephalomyelitis (EAE), auto-reactive helper T (Th) cells instigate CNS inflammation by acting on myeloid cells via the production of granulocyte-macrophage colony-stimulating factor (GM-CSF). Recent reports have implicated myeloid cells in both the inflammatory process and as executers of tissue damage in the CNS. We review these findings here, and integrate them into a model wherein GM-CSF produced by Th cells coordinates monocyte recruitment to the CNS, and differentiation into pathogenic effectors. We discuss the implications of this model to current therapies for MS, and outline important areas of further inquiry.</description><subject>Allergy and Immunology</subject><subject>Animals</subject><subject>Antigens</subject><subject>Cell Communication</subject><subject>Cell Differentiation</subject><subject>Central Nervous System Diseases - genetics</subject><subject>Central Nervous System Diseases - immunology</subject><subject>Central Nervous System Diseases - metabolism</subject><subject>Central Nervous System Diseases - pathology</subject><subject>CNS</subject><subject>Cytokines</subject><subject>Disease</subject><subject>Encephalomyelitis, Autoimmune, Experimental - genetics</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - metabolism</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>GM-CSF</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - genetics</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</subject><subject>Humans</subject><subject>Inflammation</subject><subject>Inflammation - genetics</subject><subject>Inflammation - immunology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Lymphocytes</subject><subject>monocytes</subject><subject>Multiple Sclerosis - genetics</subject><subject>Multiple Sclerosis - immunology</subject><subject>Multiple Sclerosis - metabolism</subject><subject>Multiple Sclerosis - pathology</subject><subject>Multiple Sclerosis - therapy</subject><subject>Myeloid Cells - cytology</subject><subject>Myeloid Cells - immunology</subject><subject>Myeloid Cells - metabolism</subject><subject>Neuroimmunomodulation</subject><subject>neuroinflammation</subject><subject>Studies</subject><subject>T-Lymphocytes, Helper-Inducer - immunology</subject><subject>T-Lymphocytes, Helper-Inducer - metabolism</subject><subject>Target recognition</subject><subject>tissue damage</subject><subject>Transcription factors</subject><issn>1471-4906</issn><issn>1471-4981</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kU1P3DAYhC1UVCj0zqmK1AuXBH8ltjkgoW2XVlrgAD1bXucN8jaxwU6Q9t_X6VIqceDk9_DMaDyD0AnBFcGkOdtUbqwoJnWFZYUx30OHhAtSciXJh9cbNwfoU0obnEEhxEd0QBvOiOL0EC2vrsvF3bJwvriBKQbnu94Mgxld8OfFylnwyfmH4noLfXBtsYC-T0UXYnHvUpqg-GYG8wDHaL8zfYLPL-8R-rX8fr_4Ua5ur34uLlel5YyN5VrJdQ4BhkPDTC07ZojqWFN3WHCKLWnbdUOYVLVlBqwxthFKEEw5FbJljB2h053vYwxPE6RRDy7ZnMl4CFPSRBCpCFX1jH59g27CFH1O95digjImM4V3lI0hpQidfoxuMHGrCdZzx3qj3ajnjjWWOnecJV9ejKf1AO2r4F-pGTjfAZCbeHYQdbIOvIXWRbCjboN7z_3ijdj2zjtr-t-whfT_DzpRjfXdvPE8ManzvKpR7A8s6p1e</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Croxford, Andrew L</creator><creator>Spath, Sabine</creator><creator>Becher, Burkhard</creator><general>Elsevier Ltd</general><general>Elsevier Limited</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>7U9</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>20151001</creationdate><title>GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage</title><author>Croxford, Andrew L ; Spath, Sabine ; Becher, Burkhard</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c433t-b98b015ea4e63a58f3a19f365f07420c1ddb613895c3aecaac67971024278d333</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Allergy and Immunology</topic><topic>Animals</topic><topic>Antigens</topic><topic>Cell Communication</topic><topic>Cell Differentiation</topic><topic>Central Nervous System Diseases - genetics</topic><topic>Central Nervous System Diseases - immunology</topic><topic>Central Nervous System Diseases - metabolism</topic><topic>Central Nervous System Diseases - pathology</topic><topic>CNS</topic><topic>Cytokines</topic><topic>Disease</topic><topic>Encephalomyelitis, Autoimmune, Experimental - genetics</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - metabolism</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>GM-CSF</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - genetics</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - metabolism</topic><topic>Humans</topic><topic>Inflammation</topic><topic>Inflammation - genetics</topic><topic>Inflammation - immunology</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Lymphocytes</topic><topic>monocytes</topic><topic>Multiple Sclerosis - genetics</topic><topic>Multiple Sclerosis - immunology</topic><topic>Multiple Sclerosis - metabolism</topic><topic>Multiple Sclerosis - pathology</topic><topic>Multiple Sclerosis - therapy</topic><topic>Myeloid Cells - cytology</topic><topic>Myeloid Cells - immunology</topic><topic>Myeloid Cells - metabolism</topic><topic>Neuroimmunomodulation</topic><topic>neuroinflammation</topic><topic>Studies</topic><topic>T-Lymphocytes, Helper-Inducer - immunology</topic><topic>T-Lymphocytes, Helper-Inducer - metabolism</topic><topic>Target recognition</topic><topic>tissue damage</topic><topic>Transcription factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Croxford, Andrew L</creatorcontrib><creatorcontrib>Spath, Sabine</creatorcontrib><creatorcontrib>Becher, Burkhard</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>Virology and AIDS Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Trends in immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Croxford, Andrew L</au><au>Spath, Sabine</au><au>Becher, Burkhard</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage</atitle><jtitle>Trends in immunology</jtitle><addtitle>Trends Immunol</addtitle><date>2015-10-01</date><risdate>2015</risdate><volume>36</volume><issue>10</issue><spage>651</spage><epage>662</epage><pages>651-662</pages><issn>1471-4906</issn><eissn>1471-4981</eissn><abstract>Multiple sclerosis (MS) is the prototypical inflammatory disease of the central nervous system (CNS). MS lesions harbor different immune cells, but the contribution of individual cell types to disease etiology and progression is not well understood. In experimental autoimmune encephalomyelitis (EAE), auto-reactive helper T (Th) cells instigate CNS inflammation by acting on myeloid cells via the production of granulocyte-macrophage colony-stimulating factor (GM-CSF). Recent reports have implicated myeloid cells in both the inflammatory process and as executers of tissue damage in the CNS. We review these findings here, and integrate them into a model wherein GM-CSF produced by Th cells coordinates monocyte recruitment to the CNS, and differentiation into pathogenic effectors. We discuss the implications of this model to current therapies for MS, and outline important areas of further inquiry.</abstract><cop>England</cop><pub>Elsevier Ltd</pub><pmid>26431942</pmid><doi>10.1016/j.it.2015.08.004</doi><tpages>12</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1471-4906 |
| ispartof | Trends in immunology, 2015-10, Vol.36 (10), p.651-662 |
| issn | 1471-4906 1471-4981 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1718912953 |
| source | MEDLINE; Elsevier ScienceDirect Journals |
| subjects | Allergy and Immunology Animals Antigens Cell Communication Cell Differentiation Central Nervous System Diseases - genetics Central Nervous System Diseases - immunology Central Nervous System Diseases - metabolism Central Nervous System Diseases - pathology CNS Cytokines Disease Encephalomyelitis, Autoimmune, Experimental - genetics Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - metabolism Encephalomyelitis, Autoimmune, Experimental - pathology Gene expression Gene Expression Regulation GM-CSF Granulocyte-Macrophage Colony-Stimulating Factor - genetics Granulocyte-Macrophage Colony-Stimulating Factor - metabolism Humans Inflammation Inflammation - genetics Inflammation - immunology Inflammation - metabolism Inflammation - pathology Lymphocytes monocytes Multiple Sclerosis - genetics Multiple Sclerosis - immunology Multiple Sclerosis - metabolism Multiple Sclerosis - pathology Multiple Sclerosis - therapy Myeloid Cells - cytology Myeloid Cells - immunology Myeloid Cells - metabolism Neuroimmunomodulation neuroinflammation Studies T-Lymphocytes, Helper-Inducer - immunology T-Lymphocytes, Helper-Inducer - metabolism Target recognition tissue damage Transcription factors |
| title | GM-CSF in Neuroinflammation: Licensing Myeloid Cells for Tissue Damage |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-11T23%3A56%3A07IST&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=GM-CSF%20in%20Neuroinflammation:%20Licensing%20Myeloid%20Cells%20for%20Tissue%20Damage&rft.jtitle=Trends%20in%20immunology&rft.au=Croxford,%20Andrew%20L&rft.date=2015-10-01&rft.volume=36&rft.issue=10&rft.spage=651&rft.epage=662&rft.pages=651-662&rft.issn=1471-4906&rft.eissn=1471-4981&rft_id=info:doi/10.1016/j.it.2015.08.004&rft_dat=%3Cproquest_cross%3E3824688561%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1718372338&rft_id=info:pmid/26431942&rft_els_id=1_s2_0_S1471490615001969&rfr_iscdi=true |