CCRL2 regulates M1/M2 polarization during EAE recovery phase
CCRL2 in the control of inflammation and demyelination in EAE. Chemokine (CC motif) receptor‐like 2 is a 7‐transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental auto...
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| Veröffentlicht in: | Journal of leukocyte biology 2016-06, Vol.99 (6), p.1027-1033 |
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| container_title | Journal of leukocyte biology |
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| creator | Mazzon, Cristina Zanotti, Lucia Wang, Li Del Prete, Annalisa Fontana, Elena Salvi, Valentina Poliani, Pietro Luigi Sozzani, Silvano |
| description | CCRL2 in the control of inflammation and demyelination in EAE.
Chemokine (CC motif) receptor‐like 2 is a 7‐transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental autoimmune encephalitis is an autoimmune disorder that replicates the inflammatory aspects of multiple sclerosis. Chemokine (CC motif) receptor‐like 2–deficient mice developed exacerbated, nonresolving disease with protracted inflammatory response and increased demyelination. The increased severity of the disease was associated with higher levels of microglia/macrophage activation markers and imbalanced M1/M2 polarization. Thus, chemokine (CC motif) receptor‐like 2 is involved in the downregulation of central nervous system–associated experimental autoimmune encephalitis inflammation in the recovery phase of the disease. Therefore chemokine (CC motif) receptor‐like 2 should be considered to be a molecule involved in the regulation of the inflammatory response associated with multiple sclerosis. |
| doi_str_mv | 10.1189/jlb.3MA0915-444RR |
| format | Article |
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Chemokine (CC motif) receptor‐like 2 is a 7‐transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental autoimmune encephalitis is an autoimmune disorder that replicates the inflammatory aspects of multiple sclerosis. Chemokine (CC motif) receptor‐like 2–deficient mice developed exacerbated, nonresolving disease with protracted inflammatory response and increased demyelination. The increased severity of the disease was associated with higher levels of microglia/macrophage activation markers and imbalanced M1/M2 polarization. Thus, chemokine (CC motif) receptor‐like 2 is involved in the downregulation of central nervous system–associated experimental autoimmune encephalitis inflammation in the recovery phase of the disease. Therefore chemokine (CC motif) receptor‐like 2 should be considered to be a molecule involved in the regulation of the inflammatory response associated with multiple sclerosis.</description><identifier>ISSN: 0741-5400</identifier><identifier>EISSN: 1938-3673</identifier><identifier>DOI: 10.1189/jlb.3MA0915-444RR</identifier><identifier>PMID: 26744451</identifier><language>eng</language><publisher>United States</publisher><subject>Animals ; Antigens - immunology ; atypical chemokine receptors ; Cell Polarity - drug effects ; Cell Proliferation - drug effects ; Central Nervous System - drug effects ; Central Nervous System - pathology ; chemokines ; Cross-Priming - immunology ; Disease Progression ; Encephalomyelitis, Autoimmune, Experimental - immunology ; Encephalomyelitis, Autoimmune, Experimental - pathology ; Female ; Immunization ; inflammation ; Inflammation - pathology ; Interferon-gamma - pharmacology ; macrophages ; Macrophages - drug effects ; Macrophages - metabolism ; Macrophages - pathology ; Mice, Inbred C57BL ; Mice, Knockout ; microglia ; Microglia - drug effects ; Microglia - metabolism ; multiple sclerosis ; Myelin Sheath - metabolism ; Myelin-Oligodendrocyte Glycoprotein - immunology ; Peptide Fragments - immunology ; Receptors, Chemokine - metabolism ; T-Lymphocytes - drug effects ; T-Lymphocytes - immunology</subject><ispartof>Journal of leukocyte biology, 2016-06, Vol.99 (6), p.1027-1033</ispartof><rights>2016 Society for Leukocyte Biology</rights><rights>Society for Leukocyte Biology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5387-629b729a41a4707d64933f172ae95089edb68f15e2e27b51964d4114dd3bf4273</citedby><cites>FETCH-LOGICAL-c5387-629b729a41a4707d64933f172ae95089edb68f15e2e27b51964d4114dd3bf4273</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1189%2Fjlb.3MA0915-444RR$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1189%2Fjlb.3MA0915-444RR$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26744451$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Mazzon, Cristina</creatorcontrib><creatorcontrib>Zanotti, Lucia</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Del Prete, Annalisa</creatorcontrib><creatorcontrib>Fontana, Elena</creatorcontrib><creatorcontrib>Salvi, Valentina</creatorcontrib><creatorcontrib>Poliani, Pietro Luigi</creatorcontrib><creatorcontrib>Sozzani, Silvano</creatorcontrib><title>CCRL2 regulates M1/M2 polarization during EAE recovery phase</title><title>Journal of leukocyte biology</title><addtitle>J Leukoc Biol</addtitle><description>CCRL2 in the control of inflammation and demyelination in EAE.
Chemokine (CC motif) receptor‐like 2 is a 7‐transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental autoimmune encephalitis is an autoimmune disorder that replicates the inflammatory aspects of multiple sclerosis. Chemokine (CC motif) receptor‐like 2–deficient mice developed exacerbated, nonresolving disease with protracted inflammatory response and increased demyelination. The increased severity of the disease was associated with higher levels of microglia/macrophage activation markers and imbalanced M1/M2 polarization. Thus, chemokine (CC motif) receptor‐like 2 is involved in the downregulation of central nervous system–associated experimental autoimmune encephalitis inflammation in the recovery phase of the disease. Therefore chemokine (CC motif) receptor‐like 2 should be considered to be a molecule involved in the regulation of the inflammatory response associated with multiple sclerosis.</description><subject>Animals</subject><subject>Antigens - immunology</subject><subject>atypical chemokine receptors</subject><subject>Cell Polarity - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Central Nervous System - drug effects</subject><subject>Central Nervous System - pathology</subject><subject>chemokines</subject><subject>Cross-Priming - immunology</subject><subject>Disease Progression</subject><subject>Encephalomyelitis, Autoimmune, Experimental - immunology</subject><subject>Encephalomyelitis, Autoimmune, Experimental - pathology</subject><subject>Female</subject><subject>Immunization</subject><subject>inflammation</subject><subject>Inflammation - pathology</subject><subject>Interferon-gamma - pharmacology</subject><subject>macrophages</subject><subject>Macrophages - drug effects</subject><subject>Macrophages - metabolism</subject><subject>Macrophages - pathology</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>microglia</subject><subject>Microglia - drug effects</subject><subject>Microglia - metabolism</subject><subject>multiple sclerosis</subject><subject>Myelin Sheath - metabolism</subject><subject>Myelin-Oligodendrocyte Glycoprotein - immunology</subject><subject>Peptide Fragments - immunology</subject><subject>Receptors, Chemokine - metabolism</subject><subject>T-Lymphocytes - drug effects</subject><subject>T-Lymphocytes - immunology</subject><issn>0741-5400</issn><issn>1938-3673</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkEtPwkAURidGI4j-ADemSzeFufPsJG6wwVcgJkTXk2k7xZJC6wzV4K93FHTL6m7Od5J7ELoEPARI1GhZZ0M6G2MFPGaMzedHqA-KJjEVkh6jPpYMYs4w7qEz75cYY0oEPkU9ImTgOfTRTZrOpyRydtHVZmN9NIPRjERtUxtXfZlN1ayjonPVehFNxpPA5c2HdduofTPenqOT0tTeXuzvAL3eTV7Sh3j6fP-YjqdxzmkiY0FUJokyDAyTWBaCKUpLkMRYxXGibJGJpARuiSUy46AEKxgAKwqalYxIOkDXO2_rmvfO-o1eVT63dW3Wtum8hgQnghLO2GFUKqpChpBpgGCH5q7x3tlSt65aGbfVgPVPXx366n1f_ds3bK72-i5b2eJ_8Rc0AGIHfFa13R426qfpLeDw4zdRp4QF</recordid><startdate>201606</startdate><enddate>201606</enddate><creator>Mazzon, Cristina</creator><creator>Zanotti, Lucia</creator><creator>Wang, Li</creator><creator>Del Prete, Annalisa</creator><creator>Fontana, Elena</creator><creator>Salvi, Valentina</creator><creator>Poliani, Pietro Luigi</creator><creator>Sozzani, Silvano</creator><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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201606</creationdate><title>CCRL2 regulates M1/M2 polarization during EAE recovery phase</title><author>Mazzon, Cristina ; Zanotti, Lucia ; Wang, Li ; Del Prete, Annalisa ; Fontana, Elena ; Salvi, Valentina ; Poliani, Pietro Luigi ; Sozzani, Silvano</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5387-629b729a41a4707d64933f172ae95089edb68f15e2e27b51964d4114dd3bf4273</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>Antigens - immunology</topic><topic>atypical chemokine receptors</topic><topic>Cell Polarity - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Central Nervous System - drug effects</topic><topic>Central Nervous System - pathology</topic><topic>chemokines</topic><topic>Cross-Priming - immunology</topic><topic>Disease Progression</topic><topic>Encephalomyelitis, Autoimmune, Experimental - immunology</topic><topic>Encephalomyelitis, Autoimmune, Experimental - pathology</topic><topic>Female</topic><topic>Immunization</topic><topic>inflammation</topic><topic>Inflammation - pathology</topic><topic>Interferon-gamma - pharmacology</topic><topic>macrophages</topic><topic>Macrophages - drug effects</topic><topic>Macrophages - metabolism</topic><topic>Macrophages - pathology</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>microglia</topic><topic>Microglia - drug effects</topic><topic>Microglia - metabolism</topic><topic>multiple sclerosis</topic><topic>Myelin Sheath - metabolism</topic><topic>Myelin-Oligodendrocyte Glycoprotein - immunology</topic><topic>Peptide Fragments - immunology</topic><topic>Receptors, Chemokine - metabolism</topic><topic>T-Lymphocytes - drug effects</topic><topic>T-Lymphocytes - immunology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Mazzon, Cristina</creatorcontrib><creatorcontrib>Zanotti, Lucia</creatorcontrib><creatorcontrib>Wang, Li</creatorcontrib><creatorcontrib>Del Prete, Annalisa</creatorcontrib><creatorcontrib>Fontana, Elena</creatorcontrib><creatorcontrib>Salvi, Valentina</creatorcontrib><creatorcontrib>Poliani, Pietro Luigi</creatorcontrib><creatorcontrib>Sozzani, Silvano</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Journal of leukocyte biology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Mazzon, Cristina</au><au>Zanotti, Lucia</au><au>Wang, Li</au><au>Del Prete, Annalisa</au><au>Fontana, Elena</au><au>Salvi, Valentina</au><au>Poliani, Pietro Luigi</au><au>Sozzani, Silvano</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>CCRL2 regulates M1/M2 polarization during EAE recovery phase</atitle><jtitle>Journal of leukocyte biology</jtitle><addtitle>J Leukoc Biol</addtitle><date>2016-06</date><risdate>2016</risdate><volume>99</volume><issue>6</issue><spage>1027</spage><epage>1033</epage><pages>1027-1033</pages><issn>0741-5400</issn><eissn>1938-3673</eissn><abstract>CCRL2 in the control of inflammation and demyelination in EAE.
Chemokine (CC motif) receptor‐like 2 is a 7‐transmembrane protein related to the family of the atypical chemokine receptors, which are proteins devoid of chemotactic activity and involved in the control of inflammation. Experimental autoimmune encephalitis is an autoimmune disorder that replicates the inflammatory aspects of multiple sclerosis. Chemokine (CC motif) receptor‐like 2–deficient mice developed exacerbated, nonresolving disease with protracted inflammatory response and increased demyelination. The increased severity of the disease was associated with higher levels of microglia/macrophage activation markers and imbalanced M1/M2 polarization. Thus, chemokine (CC motif) receptor‐like 2 is involved in the downregulation of central nervous system–associated experimental autoimmune encephalitis inflammation in the recovery phase of the disease. Therefore chemokine (CC motif) receptor‐like 2 should be considered to be a molecule involved in the regulation of the inflammatory response associated with multiple sclerosis.</abstract><cop>United States</cop><pmid>26744451</pmid><doi>10.1189/jlb.3MA0915-444RR</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Access via Wiley Online Library; Oxford University Press Journals All Titles (1996-Current); EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Animals Antigens - immunology atypical chemokine receptors Cell Polarity - drug effects Cell Proliferation - drug effects Central Nervous System - drug effects Central Nervous System - pathology chemokines Cross-Priming - immunology Disease Progression Encephalomyelitis, Autoimmune, Experimental - immunology Encephalomyelitis, Autoimmune, Experimental - pathology Female Immunization inflammation Inflammation - pathology Interferon-gamma - pharmacology macrophages Macrophages - drug effects Macrophages - metabolism Macrophages - pathology Mice, Inbred C57BL Mice, Knockout microglia Microglia - drug effects Microglia - metabolism multiple sclerosis Myelin Sheath - metabolism Myelin-Oligodendrocyte Glycoprotein - immunology Peptide Fragments - immunology Receptors, Chemokine - metabolism T-Lymphocytes - drug effects T-Lymphocytes - immunology |
| title | CCRL2 regulates M1/M2 polarization during EAE recovery phase |
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