Epstein–Barr virus infection negatively impacts the CXCR4‐dependent migration of tonsillar B cells
Summary The primary Epstein–Barr virus (EBV) infection occurs in the oropharynx, where the virus infects B cells and subsequently establishes latency in the memory B‐cell compartment. EBV has previously been shown to induce changes in the cell surface expression of several chemokine receptors in cel...
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| Veröffentlicht in: | Immunology 2006-03, Vol.117 (3), p.379-385 |
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| creator | Ehlin‐Henriksson, Barbro Mowafi, Frida Klein, George Nilsson, Anna |
| description | Summary
The primary Epstein–Barr virus (EBV) infection occurs in the oropharynx, where the virus infects B cells and subsequently establishes latency in the memory B‐cell compartment. EBV has previously been shown to induce changes in the cell surface expression of several chemokine receptors in cell lines and the transfection of EBNA2 or LMP1 into a B‐cell‐lymphoma‐derived cell line decreased the expression of CXCR4. We show that in vitro EBV infection reduces the expression of CXCR4 on primary tonsil B cells already 43 hr after infection. Furthermore, EBV infection affects the chemotactic response to stromal cell‐derived factor (SDF‐1)α/CXCL12, the ligand for CXCR4, with a reduction of SDF‐1α‐induced migration. To clarify whether this reduced migration is EBV‐specific or a consequence of cell activation, tonsillar B cells were either infected with EBV, activated with anti‐CD40 and interleukin‐4 (IL‐4) or kept in medium. Activation by anti‐CD40 and IL‐4 decreased the CXCR4 expression but the CD40 + IL‐4‐stimulated cells showed no reduction of chemotactic efficacy. Our finding suggests that changing the SDF‐1α response of the EBV‐infected B cells may serve the viral strategy by directing the infected cells into the extrafollicular areas, rather than retaining them in the lymphoepithelium. |
| doi_str_mv | 10.1111/j.1365-2567.2005.02311.x |
| format | Article |
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The primary Epstein–Barr virus (EBV) infection occurs in the oropharynx, where the virus infects B cells and subsequently establishes latency in the memory B‐cell compartment. EBV has previously been shown to induce changes in the cell surface expression of several chemokine receptors in cell lines and the transfection of EBNA2 or LMP1 into a B‐cell‐lymphoma‐derived cell line decreased the expression of CXCR4. We show that in vitro EBV infection reduces the expression of CXCR4 on primary tonsil B cells already 43 hr after infection. Furthermore, EBV infection affects the chemotactic response to stromal cell‐derived factor (SDF‐1)α/CXCL12, the ligand for CXCR4, with a reduction of SDF‐1α‐induced migration. To clarify whether this reduced migration is EBV‐specific or a consequence of cell activation, tonsillar B cells were either infected with EBV, activated with anti‐CD40 and interleukin‐4 (IL‐4) or kept in medium. Activation by anti‐CD40 and IL‐4 decreased the CXCR4 expression but the CD40 + IL‐4‐stimulated cells showed no reduction of chemotactic efficacy. Our finding suggests that changing the SDF‐1α response of the EBV‐infected B cells may serve the viral strategy by directing the infected cells into the extrafollicular areas, rather than retaining them in the lymphoepithelium.</description><identifier>ISSN: 0019-2805</identifier><identifier>EISSN: 1365-2567</identifier><identifier>DOI: 10.1111/j.1365-2567.2005.02311.x</identifier><identifier>PMID: 16476057</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject>B cells ; B-Lymphocytes - immunology ; CD40 Antigens - immunology ; Cells, Cultured ; Chemokine CXCL12 ; chemokines ; Chemokines, CXC - immunology ; Chemotaxis, Leukocyte - immunology ; Epstein-Barr virus ; Epstein-Barr Virus Infections - immunology ; Epstein-Barr Virus Nuclear Antigens - metabolism ; Epstein–Barr virus: migration, traffic, circulation ; Herpesvirus 4, Human - immunology ; Humans ; Interleukin-4 - immunology ; Lymphocyte Activation - immunology ; monokines ; Original ; Palatine Tonsil - immunology ; Receptors, CXCR4 - immunology ; Viral Proteins</subject><ispartof>Immunology, 2006-03, Vol.117 (3), p.379-385</ispartof><rights>Copyright Blackwell Publishing Mar 2006</rights><rights>2006 Blackwell Publishing Ltd 2006</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5681-3c1b1711cbaf37025a7548d4bddd774922cb8be8ab6c643620462cebdbbf8cc83</citedby><cites>FETCH-LOGICAL-c5681-3c1b1711cbaf37025a7548d4bddd774922cb8be8ab6c643620462cebdbbf8cc83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782227/pdf/$$EPDF$$P50$$Gpubmedcentral$$H</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC1782227/$$EHTML$$P50$$Gpubmedcentral$$H</linktohtml><link.rule.ids>230,314,550,723,776,780,881,1411,1427,27901,27902,45550,45551,46384,46808,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16476057$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttp://kipublications.ki.se/Default.aspx?queryparsed=id:1933965$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Ehlin‐Henriksson, Barbro</creatorcontrib><creatorcontrib>Mowafi, Frida</creatorcontrib><creatorcontrib>Klein, George</creatorcontrib><creatorcontrib>Nilsson, Anna</creatorcontrib><title>Epstein–Barr virus infection negatively impacts the CXCR4‐dependent migration of tonsillar B cells</title><title>Immunology</title><addtitle>Immunology</addtitle><description>Summary
The primary Epstein–Barr virus (EBV) infection occurs in the oropharynx, where the virus infects B cells and subsequently establishes latency in the memory B‐cell compartment. EBV has previously been shown to induce changes in the cell surface expression of several chemokine receptors in cell lines and the transfection of EBNA2 or LMP1 into a B‐cell‐lymphoma‐derived cell line decreased the expression of CXCR4. We show that in vitro EBV infection reduces the expression of CXCR4 on primary tonsil B cells already 43 hr after infection. Furthermore, EBV infection affects the chemotactic response to stromal cell‐derived factor (SDF‐1)α/CXCL12, the ligand for CXCR4, with a reduction of SDF‐1α‐induced migration. To clarify whether this reduced migration is EBV‐specific or a consequence of cell activation, tonsillar B cells were either infected with EBV, activated with anti‐CD40 and interleukin‐4 (IL‐4) or kept in medium. Activation by anti‐CD40 and IL‐4 decreased the CXCR4 expression but the CD40 + IL‐4‐stimulated cells showed no reduction of chemotactic efficacy. Our finding suggests that changing the SDF‐1α response of the EBV‐infected B cells may serve the viral strategy by directing the infected cells into the extrafollicular areas, rather than retaining them in the lymphoepithelium.</description><subject>B cells</subject><subject>B-Lymphocytes - immunology</subject><subject>CD40 Antigens - immunology</subject><subject>Cells, Cultured</subject><subject>Chemokine CXCL12</subject><subject>chemokines</subject><subject>Chemokines, CXC - immunology</subject><subject>Chemotaxis, Leukocyte - immunology</subject><subject>Epstein-Barr virus</subject><subject>Epstein-Barr Virus Infections - immunology</subject><subject>Epstein-Barr Virus Nuclear Antigens - metabolism</subject><subject>Epstein–Barr virus: migration, traffic, circulation</subject><subject>Herpesvirus 4, Human - immunology</subject><subject>Humans</subject><subject>Interleukin-4 - immunology</subject><subject>Lymphocyte Activation - immunology</subject><subject>monokines</subject><subject>Original</subject><subject>Palatine Tonsil - immunology</subject><subject>Receptors, CXCR4 - immunology</subject><subject>Viral Proteins</subject><issn>0019-2805</issn><issn>1365-2567</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>D8T</sourceid><recordid>eNqNUs1u1DAYtBCILguvgCwO3BL8E9vJASS6KlCpFRICiZtlO87WS-IEO9l2b30EJN6wT4LTXRXKBXzxZ38zI8_nAQBilOO0Xm1yTDnLCOMiJwixHBGKcX71ACzuGg_BAiFcZaRE7Ag8iXGTjhQx9hgcYV4IjphYgOZkiKN1_ub657EKAW5dmCJ0vrFmdL2H3q7V6La23UHXDcqMEY4XFq6-rj4VN9c_ajtYX1s_ws6tg7ql9A0cex9d26oAj6GxbRufgkeNaqN9dtiX4Mu7k8-rD9nZx_enq7dnmWG8xBk1WGOBsdGqoQIRpgQryrrQdV0LUVSEGF1qWyrNDS8oJ6jgxFhda92UxpR0CbK9bry0w6TlEFynwk72ysnD1bdUWckEr9LQluDNHp86na1NchJUe492v-PdhVz3W4lFSQgRSeDlQSD03ycbR9m5OFtW3vZTlFxwnr6E_hOYbAtK0GzhxV_ATT8Fn6YmcVUVhDOBEqjcg0zoYwy2uXsyRnKOiNzIOQlyToKcIyJvIyKvEvX5n5Z_Ew-ZSIDXe8Cla-3uv4Xl6fn5XNFfab3Ogw</recordid><startdate>200603</startdate><enddate>200603</enddate><creator>Ehlin‐Henriksson, Barbro</creator><creator>Mowafi, Frida</creator><creator>Klein, George</creator><creator>Nilsson, Anna</creator><general>Blackwell Publishing Ltd</general><general>Wiley Subscription Services, Inc</general><general>Blackwell Science Inc</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>7QL</scope><scope>7QR</scope><scope>7T5</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>5PM</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>D8T</scope><scope>ZZAVC</scope></search><sort><creationdate>200603</creationdate><title>Epstein–Barr virus infection negatively impacts the CXCR4‐dependent migration of tonsillar B cells</title><author>Ehlin‐Henriksson, Barbro ; Mowafi, Frida ; Klein, George ; Nilsson, Anna</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5681-3c1b1711cbaf37025a7548d4bddd774922cb8be8ab6c643620462cebdbbf8cc83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>B cells</topic><topic>B-Lymphocytes - immunology</topic><topic>CD40 Antigens - immunology</topic><topic>Cells, Cultured</topic><topic>Chemokine CXCL12</topic><topic>chemokines</topic><topic>Chemokines, CXC - immunology</topic><topic>Chemotaxis, Leukocyte - immunology</topic><topic>Epstein-Barr virus</topic><topic>Epstein-Barr Virus Infections - immunology</topic><topic>Epstein-Barr Virus Nuclear Antigens - metabolism</topic><topic>Epstein–Barr virus: migration, traffic, circulation</topic><topic>Herpesvirus 4, Human - immunology</topic><topic>Humans</topic><topic>Interleukin-4 - immunology</topic><topic>Lymphocyte Activation - immunology</topic><topic>monokines</topic><topic>Original</topic><topic>Palatine Tonsil - immunology</topic><topic>Receptors, CXCR4 - immunology</topic><topic>Viral Proteins</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ehlin‐Henriksson, Barbro</creatorcontrib><creatorcontrib>Mowafi, Frida</creatorcontrib><creatorcontrib>Klein, George</creatorcontrib><creatorcontrib>Nilsson, Anna</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Chemoreception Abstracts</collection><collection>Immunology Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Freely available online</collection><collection>SwePub Articles full text</collection><jtitle>Immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ehlin‐Henriksson, Barbro</au><au>Mowafi, Frida</au><au>Klein, George</au><au>Nilsson, Anna</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Epstein–Barr virus infection negatively impacts the CXCR4‐dependent migration of tonsillar B cells</atitle><jtitle>Immunology</jtitle><addtitle>Immunology</addtitle><date>2006-03</date><risdate>2006</risdate><volume>117</volume><issue>3</issue><spage>379</spage><epage>385</epage><pages>379-385</pages><issn>0019-2805</issn><eissn>1365-2567</eissn><abstract>Summary
The primary Epstein–Barr virus (EBV) infection occurs in the oropharynx, where the virus infects B cells and subsequently establishes latency in the memory B‐cell compartment. EBV has previously been shown to induce changes in the cell surface expression of several chemokine receptors in cell lines and the transfection of EBNA2 or LMP1 into a B‐cell‐lymphoma‐derived cell line decreased the expression of CXCR4. We show that in vitro EBV infection reduces the expression of CXCR4 on primary tonsil B cells already 43 hr after infection. Furthermore, EBV infection affects the chemotactic response to stromal cell‐derived factor (SDF‐1)α/CXCL12, the ligand for CXCR4, with a reduction of SDF‐1α‐induced migration. To clarify whether this reduced migration is EBV‐specific or a consequence of cell activation, tonsillar B cells were either infected with EBV, activated with anti‐CD40 and interleukin‐4 (IL‐4) or kept in medium. Activation by anti‐CD40 and IL‐4 decreased the CXCR4 expression but the CD40 + IL‐4‐stimulated cells showed no reduction of chemotactic efficacy. Our finding suggests that changing the SDF‐1α response of the EBV‐infected B cells may serve the viral strategy by directing the infected cells into the extrafollicular areas, rather than retaining them in the lymphoepithelium.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>16476057</pmid><doi>10.1111/j.1365-2567.2005.02311.x</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | B cells B-Lymphocytes - immunology CD40 Antigens - immunology Cells, Cultured Chemokine CXCL12 chemokines Chemokines, CXC - immunology Chemotaxis, Leukocyte - immunology Epstein-Barr virus Epstein-Barr Virus Infections - immunology Epstein-Barr Virus Nuclear Antigens - metabolism Epstein–Barr virus: migration, traffic, circulation Herpesvirus 4, Human - immunology Humans Interleukin-4 - immunology Lymphocyte Activation - immunology monokines Original Palatine Tonsil - immunology Receptors, CXCR4 - immunology Viral Proteins |
| title | Epstein–Barr virus infection negatively impacts the CXCR4‐dependent migration of tonsillar B cells |
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