Dendritic cells and regulatory T cells expressing CCR4 provide resistance to coxsackievirus B5-induced pancreatitis
Type B coxsackieviruses (CVB) are enteroviruses responsible for a common infectious myocarditis and pancreatitis. DCs and regulatory T cells (Tregs) are key players in controlling virus replication and regulating the immune response and tissue damage, respectively. However, the mechanisms underlying...
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| Veröffentlicht in: | Scientific reports 2019-10, Vol.9 (1), p.14766-11, Article 14766 |
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| creator | Françozo, Marcela C. S. Costa, Frederico R. C. Guerra-Gomes, Isabel C. Silva, João S. Sesti-Costa, Renata |
| description | Type B coxsackieviruses (CVB) are enteroviruses responsible for a common infectious myocarditis and pancreatitis. DCs and regulatory T cells (Tregs) are key players in controlling virus replication and regulating the immune response and tissue damage, respectively. However, the mechanisms underlying cellular migration to target tissues remain unclear. In the present study, we found that CVB5 infection induced CCL17 production and controlled the migration of CCR4
+
DCs and CCR4
+
Tregs to the pancreatic lymph nodes (pLN). CVB5 infection of CCR4
−/−
mice reduced the migration of the CD8α
+
DC subset and reduced DC activation and production of IFN-β and IL-12. Consequently, CCR4
−/−
mice presented decreased IFN-γ-producing CD4
+
and CD8
+
T cells, an increased viral load and more severe pancreatitis. In addition, CCR4
−/−
mice had impaired Treg accumulation in pLN as well as increased T lymphocyte activation. Adoptive transfer of CCR4
+
Tregs but not CCR4
−
Tregs was able to regulate T lymphocyte activation upon CVB5 infection. The present data reveal a previously unknown role for CCR4 in coordinating immune cell migration to CVB-infected tissues and in controlling subsequent pancreatitis. These new insights may contribute to the design of future therapies for acute and chronic infection of non-polio enteroviruses. |
| doi_str_mv | 10.1038/s41598-019-51311-9 |
| format | Article |
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+
DCs and CCR4
+
Tregs to the pancreatic lymph nodes (pLN). CVB5 infection of CCR4
−/−
mice reduced the migration of the CD8α
+
DC subset and reduced DC activation and production of IFN-β and IL-12. Consequently, CCR4
−/−
mice presented decreased IFN-γ-producing CD4
+
and CD8
+
T cells, an increased viral load and more severe pancreatitis. In addition, CCR4
−/−
mice had impaired Treg accumulation in pLN as well as increased T lymphocyte activation. Adoptive transfer of CCR4
+
Tregs but not CCR4
−
Tregs was able to regulate T lymphocyte activation upon CVB5 infection. The present data reveal a previously unknown role for CCR4 in coordinating immune cell migration to CVB-infected tissues and in controlling subsequent pancreatitis. These new insights may contribute to the design of future therapies for acute and chronic infection of non-polio enteroviruses.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-51311-9</identifier><identifier>PMID: 31611578</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>13 ; 13/21 ; 13/31 ; 38 ; 38/77 ; 631/250/2499 ; 631/250/2504/133/2505 ; 631/250/98 ; 64/60 ; 692/699/255/2514 ; 82 ; 82/51 ; Adoptive transfer ; Animals ; CCL17 protein ; CD4 antigen ; CD8 antigen ; Cell activation ; Cell adhesion & migration ; Cell Movement ; Chemokine CCL17 - immunology ; Chronic infection ; Coxsackievirus Infections - complications ; Coxsackievirus Infections - immunology ; Coxsackievirus Infections - pathology ; Coxsackieviruses ; Dendritic cells ; Dendritic Cells - immunology ; Dendritic Cells - pathology ; Enterovirus B, Human - immunology ; Heart diseases ; Humanities and Social Sciences ; Immune response ; Immunoregulation ; Infections ; Interleukin 12 ; Leukocyte migration ; Lymph nodes ; Lymphocytes ; Lymphocytes T ; Mice, Inbred C57BL ; multidisciplinary ; Myocarditis ; Pancreas ; Pancreatitis ; Pancreatitis - etiology ; Pancreatitis - immunology ; Pancreatitis - pathology ; Pancreatitis - virology ; Receptors, CCR4 - immunology ; Science ; Science (multidisciplinary) ; T-Lymphocytes, Regulatory - immunology ; T-Lymphocytes, Regulatory - pathology ; β-Interferon ; γ-Interferon</subject><ispartof>Scientific reports, 2019-10, Vol.9 (1), p.14766-11, Article 14766</ispartof><rights>The Author(s) 2019</rights><rights>2019. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-755efc53588abf29ec64bbbc6c5613a692abdc157beb0190c5c37015ee3099783</citedby><cites>FETCH-LOGICAL-c474t-755efc53588abf29ec64bbbc6c5613a692abdc157beb0190c5c37015ee3099783</cites><orcidid>0000-0002-7098-2850 ; 0000-0001-8436-9830</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791842/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6791842/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,27901,27902,41096,42165,51551,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31611578$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Françozo, Marcela C. S.</creatorcontrib><creatorcontrib>Costa, Frederico R. C.</creatorcontrib><creatorcontrib>Guerra-Gomes, Isabel C.</creatorcontrib><creatorcontrib>Silva, João S.</creatorcontrib><creatorcontrib>Sesti-Costa, Renata</creatorcontrib><title>Dendritic cells and regulatory T cells expressing CCR4 provide resistance to coxsackievirus B5-induced pancreatitis</title><title>Scientific reports</title><addtitle>Sci Rep</addtitle><addtitle>Sci Rep</addtitle><description>Type B coxsackieviruses (CVB) are enteroviruses responsible for a common infectious myocarditis and pancreatitis. DCs and regulatory T cells (Tregs) are key players in controlling virus replication and regulating the immune response and tissue damage, respectively. However, the mechanisms underlying cellular migration to target tissues remain unclear. In the present study, we found that CVB5 infection induced CCL17 production and controlled the migration of CCR4
+
DCs and CCR4
+
Tregs to the pancreatic lymph nodes (pLN). CVB5 infection of CCR4
−/−
mice reduced the migration of the CD8α
+
DC subset and reduced DC activation and production of IFN-β and IL-12. Consequently, CCR4
−/−
mice presented decreased IFN-γ-producing CD4
+
and CD8
+
T cells, an increased viral load and more severe pancreatitis. In addition, CCR4
−/−
mice had impaired Treg accumulation in pLN as well as increased T lymphocyte activation. Adoptive transfer of CCR4
+
Tregs but not CCR4
−
Tregs was able to regulate T lymphocyte activation upon CVB5 infection. The present data reveal a previously unknown role for CCR4 in coordinating immune cell migration to CVB-infected tissues and in controlling subsequent pancreatitis. These new insights may contribute to the design of future therapies for acute and chronic infection of non-polio enteroviruses.</description><subject>13</subject><subject>13/21</subject><subject>13/31</subject><subject>38</subject><subject>38/77</subject><subject>631/250/2499</subject><subject>631/250/2504/133/2505</subject><subject>631/250/98</subject><subject>64/60</subject><subject>692/699/255/2514</subject><subject>82</subject><subject>82/51</subject><subject>Adoptive transfer</subject><subject>Animals</subject><subject>CCL17 protein</subject><subject>CD4 antigen</subject><subject>CD8 antigen</subject><subject>Cell activation</subject><subject>Cell adhesion & migration</subject><subject>Cell Movement</subject><subject>Chemokine CCL17 - immunology</subject><subject>Chronic infection</subject><subject>Coxsackievirus Infections - complications</subject><subject>Coxsackievirus Infections - immunology</subject><subject>Coxsackievirus Infections - pathology</subject><subject>Coxsackieviruses</subject><subject>Dendritic cells</subject><subject>Dendritic Cells - immunology</subject><subject>Dendritic Cells - pathology</subject><subject>Enterovirus B, Human - immunology</subject><subject>Heart diseases</subject><subject>Humanities and Social Sciences</subject><subject>Immune response</subject><subject>Immunoregulation</subject><subject>Infections</subject><subject>Interleukin 12</subject><subject>Leukocyte migration</subject><subject>Lymph nodes</subject><subject>Lymphocytes</subject><subject>Lymphocytes T</subject><subject>Mice, Inbred C57BL</subject><subject>multidisciplinary</subject><subject>Myocarditis</subject><subject>Pancreas</subject><subject>Pancreatitis</subject><subject>Pancreatitis - etiology</subject><subject>Pancreatitis - immunology</subject><subject>Pancreatitis - pathology</subject><subject>Pancreatitis - virology</subject><subject>Receptors, CCR4 - immunology</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>T-Lymphocytes, Regulatory - immunology</subject><subject>T-Lymphocytes, Regulatory - pathology</subject><subject>β-Interferon</subject><subject>γ-Interferon</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUtv1DAUhS0EolXpH-iistQNm4CfSbypBAO0SJWQULu2HOfO4JKxU99k1P573M70AQu8seX7-Vyfewg54uwDZ7L9iIpr01aMm0pzyXllXpF9wZSuhBTi9YvzHjlEvGZlaWEUN2_JnuQ157pp9wl-gdjnMAVPPQwDUhd7mmE1D25K-Y5e7q7hdsyAGOKKLhY_FR1z2oQeCooBJxc90ClRn27R-d8BNiHPSD_rKsR-9tDTsSAZ3FQ64TvyZukGhMPdfkCuvn29XJxXFz_Ovi8-XVReNWqqGq1h6bXUbeu6pTDga9V1na-9rrl0tRGu632x0UFXxsC89rJhXANIZkzTygNyutUd524NvYc4ZTfYMYe1y3c2uWD_rsTwy67SxtaN4a0SReD9TiCnmxlwsuuA9_NwEdKMVkimG2O4lAU9-Qe9TnOOxd4DpWVdK1UosaV8TogZlk-f4czex2q3sdrixz7Eak15dPzSxtOTxxALILcAllJcQX7u_R_ZPwV9r5k</recordid><startdate>20191014</startdate><enddate>20191014</enddate><creator>Françozo, Marcela C. 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C. ; Guerra-Gomes, Isabel C. ; Silva, João S. ; Sesti-Costa, Renata</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-755efc53588abf29ec64bbbc6c5613a692abdc157beb0190c5c37015ee3099783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>13</topic><topic>13/21</topic><topic>13/31</topic><topic>38</topic><topic>38/77</topic><topic>631/250/2499</topic><topic>631/250/2504/133/2505</topic><topic>631/250/98</topic><topic>64/60</topic><topic>692/699/255/2514</topic><topic>82</topic><topic>82/51</topic><topic>Adoptive transfer</topic><topic>Animals</topic><topic>CCL17 protein</topic><topic>CD4 antigen</topic><topic>CD8 antigen</topic><topic>Cell activation</topic><topic>Cell adhesion & migration</topic><topic>Cell Movement</topic><topic>Chemokine CCL17 - immunology</topic><topic>Chronic infection</topic><topic>Coxsackievirus Infections - complications</topic><topic>Coxsackievirus Infections - immunology</topic><topic>Coxsackievirus Infections - pathology</topic><topic>Coxsackieviruses</topic><topic>Dendritic cells</topic><topic>Dendritic Cells - immunology</topic><topic>Dendritic Cells - pathology</topic><topic>Enterovirus B, Human - immunology</topic><topic>Heart diseases</topic><topic>Humanities and Social Sciences</topic><topic>Immune response</topic><topic>Immunoregulation</topic><topic>Infections</topic><topic>Interleukin 12</topic><topic>Leukocyte migration</topic><topic>Lymph nodes</topic><topic>Lymphocytes</topic><topic>Lymphocytes T</topic><topic>Mice, Inbred C57BL</topic><topic>multidisciplinary</topic><topic>Myocarditis</topic><topic>Pancreas</topic><topic>Pancreatitis</topic><topic>Pancreatitis - etiology</topic><topic>Pancreatitis - immunology</topic><topic>Pancreatitis - pathology</topic><topic>Pancreatitis - virology</topic><topic>Receptors, CCR4 - immunology</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>T-Lymphocytes, Regulatory - immunology</topic><topic>T-Lymphocytes, Regulatory - pathology</topic><topic>β-Interferon</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Françozo, Marcela C. S.</creatorcontrib><creatorcontrib>Costa, Frederico R. C.</creatorcontrib><creatorcontrib>Guerra-Gomes, Isabel C.</creatorcontrib><creatorcontrib>Silva, João S.</creatorcontrib><creatorcontrib>Sesti-Costa, Renata</creatorcontrib><collection>Springer Nature OA Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</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 One Sustainability</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>Publicly Available Content 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 Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Françozo, Marcela C. S.</au><au>Costa, Frederico R. C.</au><au>Guerra-Gomes, Isabel C.</au><au>Silva, João S.</au><au>Sesti-Costa, Renata</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dendritic cells and regulatory T cells expressing CCR4 provide resistance to coxsackievirus B5-induced pancreatitis</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-10-14</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>14766</spage><epage>11</epage><pages>14766-11</pages><artnum>14766</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Type B coxsackieviruses (CVB) are enteroviruses responsible for a common infectious myocarditis and pancreatitis. DCs and regulatory T cells (Tregs) are key players in controlling virus replication and regulating the immune response and tissue damage, respectively. However, the mechanisms underlying cellular migration to target tissues remain unclear. In the present study, we found that CVB5 infection induced CCL17 production and controlled the migration of CCR4
+
DCs and CCR4
+
Tregs to the pancreatic lymph nodes (pLN). CVB5 infection of CCR4
−/−
mice reduced the migration of the CD8α
+
DC subset and reduced DC activation and production of IFN-β and IL-12. Consequently, CCR4
−/−
mice presented decreased IFN-γ-producing CD4
+
and CD8
+
T cells, an increased viral load and more severe pancreatitis. In addition, CCR4
−/−
mice had impaired Treg accumulation in pLN as well as increased T lymphocyte activation. Adoptive transfer of CCR4
+
Tregs but not CCR4
−
Tregs was able to regulate T lymphocyte activation upon CVB5 infection. The present data reveal a previously unknown role for CCR4 in coordinating immune cell migration to CVB-infected tissues and in controlling subsequent pancreatitis. These new insights may contribute to the design of future therapies for acute and chronic infection of non-polio enteroviruses.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31611578</pmid><doi>10.1038/s41598-019-51311-9</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-7098-2850</orcidid><orcidid>https://orcid.org/0000-0001-8436-9830</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Nature Free; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; Free Full-Text Journals in Chemistry; Springer Nature OA Free Journals |
| subjects | 13 13/21 13/31 38 38/77 631/250/2499 631/250/2504/133/2505 631/250/98 64/60 692/699/255/2514 82 82/51 Adoptive transfer Animals CCL17 protein CD4 antigen CD8 antigen Cell activation Cell adhesion & migration Cell Movement Chemokine CCL17 - immunology Chronic infection Coxsackievirus Infections - complications Coxsackievirus Infections - immunology Coxsackievirus Infections - pathology Coxsackieviruses Dendritic cells Dendritic Cells - immunology Dendritic Cells - pathology Enterovirus B, Human - immunology Heart diseases Humanities and Social Sciences Immune response Immunoregulation Infections Interleukin 12 Leukocyte migration Lymph nodes Lymphocytes Lymphocytes T Mice, Inbred C57BL multidisciplinary Myocarditis Pancreas Pancreatitis Pancreatitis - etiology Pancreatitis - immunology Pancreatitis - pathology Pancreatitis - virology Receptors, CCR4 - immunology Science Science (multidisciplinary) T-Lymphocytes, Regulatory - immunology T-Lymphocytes, Regulatory - pathology β-Interferon γ-Interferon |
| title | Dendritic cells and regulatory T cells expressing CCR4 provide resistance to coxsackievirus B5-induced pancreatitis |
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