Fewer CTL, not enhanced NK cells, are sufficient for viral clearance from the lungs of immunocompromised mice
Activation of the aryl hydrocarbon receptor (AhR) causes numerous defects in anti-viral immunity, including suppressed CTL generation and impaired host resistance. However, despite a reduced CTL response, mice that survive infection clear the virus. Therefore, we examined the contribution of NK cell...
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Veröffentlicht in: | Cellular immunology 2003-11, Vol.226 (1), p.54-64 |
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description | Activation of the aryl hydrocarbon receptor (AhR) causes numerous defects in anti-viral immunity, including suppressed CTL generation and impaired host resistance. However, despite a reduced CTL response, mice that survive infection clear the virus. Therefore, we examined the contribution of NK cells and pro-inflammatory cytokines to viral clearance in influenza virus-infected mice exposed to TCDD, the most potent AhR agonist. Infection caused transient increases in pulmonary TNFα, IL-1, and IFNα/β levels, but neither the kinetics nor magnitude of this response was affected by AhR activation. No IL-18 was detected at any time point examined. Exposure to TCDD enhanced NK cell numbers in the lung but did not affect their IFNγ production. Furthermore, depletion of NK cells did not alter anti-viral cytolytic activity. In contrast, removal of CD8
+ T cells ablated virus-specific cytolytic activity. These results demonstrate that the pulmonary CTL response to influenza virus is robust and few CTL are necessary for viral clearance. |
doi_str_mv | 10.1016/j.cellimm.2003.11.005 |
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+ T cells ablated virus-specific cytolytic activity. These results demonstrate that the pulmonary CTL response to influenza virus is robust and few CTL are necessary for viral clearance.</description><identifier>ISSN: 0008-8749</identifier><identifier>EISSN: 1090-2163</identifier><identifier>DOI: 10.1016/j.cellimm.2003.11.005</identifier><identifier>PMID: 14746808</identifier><language>eng</language><publisher>Netherlands: Elsevier Inc</publisher><subject>Ah receptor ; Animals ; Anti-viral immunity ; Bronchoalveolar Lavage Fluid - cytology ; CD8 Antigens - metabolism ; CTL ; Cytokines ; Dioxin (TCDD) ; Female ; IFNγ ; Immune suppression ; In vivo ; Influenza A virus - immunology ; Influenza A virus - metabolism ; Influenza virus ; Interferon-gamma - immunology ; Killer Cells, Natural - immunology ; Lung - immunology ; Lung - virology ; Mice ; Mice, Inbred C57BL ; NK cells ; Orthomyxoviridae Infections - immunology ; Polychlorinated Dibenzodioxins - metabolism ; Receptors, Aryl Hydrocarbon - immunology ; Receptors, Aryl Hydrocarbon - metabolism ; T-Lymphocytes, Cytotoxic - immunology ; Teratogens - metabolism</subject><ispartof>Cellular immunology, 2003-11, Vol.226 (1), p.54-64</ispartof><rights>2003 Elsevier Inc.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-1d9e382d0b465f92d96377ccc9c538ce0bfee6ae9e93d7c806730fb234ea58d23</citedby><cites>FETCH-LOGICAL-c392t-1d9e382d0b465f92d96377ccc9c538ce0bfee6ae9e93d7c806730fb234ea58d23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0008874903002685$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14746808$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Neff-LaFord, Haley D.</creatorcontrib><creatorcontrib>Vorderstrasse, Beth A.</creatorcontrib><creatorcontrib>Lawrence, B.Paige</creatorcontrib><title>Fewer CTL, not enhanced NK cells, are sufficient for viral clearance from the lungs of immunocompromised mice</title><title>Cellular immunology</title><addtitle>Cell Immunol</addtitle><description>Activation of the aryl hydrocarbon receptor (AhR) causes numerous defects in anti-viral immunity, including suppressed CTL generation and impaired host resistance. However, despite a reduced CTL response, mice that survive infection clear the virus. Therefore, we examined the contribution of NK cells and pro-inflammatory cytokines to viral clearance in influenza virus-infected mice exposed to TCDD, the most potent AhR agonist. Infection caused transient increases in pulmonary TNFα, IL-1, and IFNα/β levels, but neither the kinetics nor magnitude of this response was affected by AhR activation. No IL-18 was detected at any time point examined. Exposure to TCDD enhanced NK cell numbers in the lung but did not affect their IFNγ production. Furthermore, depletion of NK cells did not alter anti-viral cytolytic activity. In contrast, removal of CD8
+ T cells ablated virus-specific cytolytic activity. These results demonstrate that the pulmonary CTL response to influenza virus is robust and few CTL are necessary for viral clearance.</description><subject>Ah receptor</subject><subject>Animals</subject><subject>Anti-viral immunity</subject><subject>Bronchoalveolar Lavage Fluid - cytology</subject><subject>CD8 Antigens - metabolism</subject><subject>CTL</subject><subject>Cytokines</subject><subject>Dioxin (TCDD)</subject><subject>Female</subject><subject>IFNγ</subject><subject>Immune suppression</subject><subject>In vivo</subject><subject>Influenza A virus - immunology</subject><subject>Influenza A virus - metabolism</subject><subject>Influenza virus</subject><subject>Interferon-gamma - immunology</subject><subject>Killer Cells, Natural - immunology</subject><subject>Lung - immunology</subject><subject>Lung - virology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NK cells</subject><subject>Orthomyxoviridae Infections - immunology</subject><subject>Polychlorinated Dibenzodioxins - metabolism</subject><subject>Receptors, Aryl Hydrocarbon - immunology</subject><subject>Receptors, Aryl Hydrocarbon - metabolism</subject><subject>T-Lymphocytes, Cytotoxic - immunology</subject><subject>Teratogens - metabolism</subject><issn>0008-8749</issn><issn>1090-2163</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2003</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMFO3DAQhi1UBNuFR2jlU0-bMI4TJz6halVoxQouy9nyOmPwKonBThb17XG0K_XY0xzmm_lnPkK-McgZMHGzzw12nev7vADgOWM5QHVGFgwkZAUT_AtZAECTNXUpL8nXGPcAjJUSLsglK-tSNNAsSH-HHxjoertZ0cGPFIdXPRhs6eMDnQPiiuqANE7WOuNwGKn1gR5c0B01Heow09QG39PxFWk3DS-RekvTYdPgje_fUsvFtLB3Bq_IudVdxOtTXZLnu1_b9e9s83T_Z_1zkxkuizFjrUTeFC3sSlFZWbRS8Lo2xkhT8cYg7Cyi0ChR8rY2DYiag90VvERdNW3Bl-THcW9Kf58wjirdML-jB_RTVKyWlRBVmcDqCJrgYwxo1VtwvQ5_FQM1e1Z7dfKsZs-KMZU8p7nvp4Bp12P7b-okNgG3RwDTmweHQcVZXzLrAppRtd79J-ITNi6SIg</recordid><startdate>20031101</startdate><enddate>20031101</enddate><creator>Neff-LaFord, Haley D.</creator><creator>Vorderstrasse, Beth A.</creator><creator>Lawrence, B.Paige</creator><general>Elsevier 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>7T5</scope><scope>7U9</scope><scope>H94</scope></search><sort><creationdate>20031101</creationdate><title>Fewer CTL, not enhanced NK cells, are sufficient for viral clearance from the lungs of immunocompromised mice</title><author>Neff-LaFord, Haley D. ; Vorderstrasse, Beth A. ; Lawrence, B.Paige</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-1d9e382d0b465f92d96377ccc9c538ce0bfee6ae9e93d7c806730fb234ea58d23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2003</creationdate><topic>Ah receptor</topic><topic>Animals</topic><topic>Anti-viral immunity</topic><topic>Bronchoalveolar Lavage Fluid - cytology</topic><topic>CD8 Antigens - metabolism</topic><topic>CTL</topic><topic>Cytokines</topic><topic>Dioxin (TCDD)</topic><topic>Female</topic><topic>IFNγ</topic><topic>Immune suppression</topic><topic>In vivo</topic><topic>Influenza A virus - immunology</topic><topic>Influenza A virus - metabolism</topic><topic>Influenza virus</topic><topic>Interferon-gamma - immunology</topic><topic>Killer Cells, Natural - immunology</topic><topic>Lung - immunology</topic><topic>Lung - virology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NK cells</topic><topic>Orthomyxoviridae Infections - immunology</topic><topic>Polychlorinated Dibenzodioxins - metabolism</topic><topic>Receptors, Aryl Hydrocarbon - immunology</topic><topic>Receptors, Aryl Hydrocarbon - metabolism</topic><topic>T-Lymphocytes, Cytotoxic - immunology</topic><topic>Teratogens - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Neff-LaFord, Haley D.</creatorcontrib><creatorcontrib>Vorderstrasse, Beth A.</creatorcontrib><creatorcontrib>Lawrence, B.Paige</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><jtitle>Cellular immunology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Neff-LaFord, Haley D.</au><au>Vorderstrasse, Beth A.</au><au>Lawrence, B.Paige</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Fewer CTL, not enhanced NK cells, are sufficient for viral clearance from the lungs of immunocompromised mice</atitle><jtitle>Cellular immunology</jtitle><addtitle>Cell Immunol</addtitle><date>2003-11-01</date><risdate>2003</risdate><volume>226</volume><issue>1</issue><spage>54</spage><epage>64</epage><pages>54-64</pages><issn>0008-8749</issn><eissn>1090-2163</eissn><abstract>Activation of the aryl hydrocarbon receptor (AhR) causes numerous defects in anti-viral immunity, including suppressed CTL generation and impaired host resistance. However, despite a reduced CTL response, mice that survive infection clear the virus. Therefore, we examined the contribution of NK cells and pro-inflammatory cytokines to viral clearance in influenza virus-infected mice exposed to TCDD, the most potent AhR agonist. Infection caused transient increases in pulmonary TNFα, IL-1, and IFNα/β levels, but neither the kinetics nor magnitude of this response was affected by AhR activation. No IL-18 was detected at any time point examined. Exposure to TCDD enhanced NK cell numbers in the lung but did not affect their IFNγ production. Furthermore, depletion of NK cells did not alter anti-viral cytolytic activity. In contrast, removal of CD8
+ T cells ablated virus-specific cytolytic activity. These results demonstrate that the pulmonary CTL response to influenza virus is robust and few CTL are necessary for viral clearance.</abstract><cop>Netherlands</cop><pub>Elsevier Inc</pub><pmid>14746808</pmid><doi>10.1016/j.cellimm.2003.11.005</doi><tpages>11</tpages></addata></record> |
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subjects | Ah receptor Animals Anti-viral immunity Bronchoalveolar Lavage Fluid - cytology CD8 Antigens - metabolism CTL Cytokines Dioxin (TCDD) Female IFNγ Immune suppression In vivo Influenza A virus - immunology Influenza A virus - metabolism Influenza virus Interferon-gamma - immunology Killer Cells, Natural - immunology Lung - immunology Lung - virology Mice Mice, Inbred C57BL NK cells Orthomyxoviridae Infections - immunology Polychlorinated Dibenzodioxins - metabolism Receptors, Aryl Hydrocarbon - immunology Receptors, Aryl Hydrocarbon - metabolism T-Lymphocytes, Cytotoxic - immunology Teratogens - metabolism |
title | Fewer CTL, not enhanced NK cells, are sufficient for viral clearance from the lungs of immunocompromised mice |
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