Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection
Mice infected with mouse hepatitis virus A59 (MHV-A59) develop hepatitis and autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH), a fact closely related to the release of alarmins such as uric acid and/or high-mobility group box protein 1 (HMGB1). We studied the effect of...
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| Veröffentlicht in: | European cytokine network 2017-09, Vol.28 (3), p.111-119 |
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| creator | Aparicio, José L Ottobre, Macarena Duhalde Vega, Maite Coutelier, Jean-Paul Van Snick, Jacques Retegui, Lilia A |
| description | Mice infected with mouse hepatitis virus A59 (MHV-A59) develop hepatitis and autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH), a fact closely related to the release of alarmins such as uric acid and/or high-mobility group box protein 1 (HMGB1). We studied the effect of neutralizing monoclonal antibodies (MAb) against IL-17A in our model of mouse MHV-A59-infection. MAb anti-IL-17F and anti-IFNγ were used to complement the study. Results showed that transaminase levels markedly decreased in MHV-A59-infected mice treated with MAb anti-IL-17A whereas plasmatic Ig concentration sharply increased. Conversely, MAb anti-IL-17F enhanced transaminase liberation and did not affect Ig levels. Serum IFNγ was detected in mice infected with MHV-A59 and its concentration increased after MAb anti-IL-17A administration. Besides, MAb anti-IFNγ greatly augmented transaminase plasmatic levels. IL-17A neutralization did not affect MHV-A59-induction of HMGB1 liberation and slightly augmented plasmatic uric acid concentration. However, mice treated with the MAb failed to produce autoAb to FAH. The above results suggest a reciprocal regulation of Th1 and Th17 cells acting on the different MHV-A59 effects. In addition, it is proposed that IL-17A is involved in alarmins adjuvant effects leading to autoAb expression. |
| doi_str_mv | 10.1684/ecn.2017.0399 |
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We studied the effect of neutralizing monoclonal antibodies (MAb) against IL-17A in our model of mouse MHV-A59-infection. MAb anti-IL-17F and anti-IFNγ were used to complement the study. Results showed that transaminase levels markedly decreased in MHV-A59-infected mice treated with MAb anti-IL-17A whereas plasmatic Ig concentration sharply increased. Conversely, MAb anti-IL-17F enhanced transaminase liberation and did not affect Ig levels. Serum IFNγ was detected in mice infected with MHV-A59 and its concentration increased after MAb anti-IL-17A administration. Besides, MAb anti-IFNγ greatly augmented transaminase plasmatic levels. IL-17A neutralization did not affect MHV-A59-induction of HMGB1 liberation and slightly augmented plasmatic uric acid concentration. However, mice treated with the MAb failed to produce autoAb to FAH. The above results suggest a reciprocal regulation of Th1 and Th17 cells acting on the different MHV-A59 effects. In addition, it is proposed that IL-17A is involved in alarmins adjuvant effects leading to autoAb expression.</description><identifier>ISSN: 1148-5493</identifier><identifier>EISSN: 1952-4005</identifier><identifier>DOI: 10.1684/ecn.2017.0399</identifier><identifier>PMID: 29187338</identifier><language>eng</language><publisher>France: Springer Nature B.V</publisher><subject>Animals ; Autoantibodies ; Autoantibodies - immunology ; Cell Differentiation - physiology ; Female ; Fumarylacetoacetase ; Helper cells ; Hepatitis ; HMGB1 protein ; Hydrolases - metabolism ; Immunoglobulins ; Interleukin-17 - metabolism ; Kidney - metabolism ; Kidneys ; Liver ; Liver - metabolism ; Lymphocytes T ; Mice ; Monoclonal antibodies ; Murine hepatitis virus - immunology ; Murine hepatitis virus - metabolism ; Murine hepatitis virus - pathogenicity ; Transaminase ; Uric acid ; γ-Interferon</subject><ispartof>European cytokine network, 2017-09, Vol.28 (3), p.111-119</ispartof><rights>2017© John Libbey Eurotext 2017</rights><rights>John Libbey Eurotext 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c454t-b8db5ff8a15908a495df967a78bc9f6c99ad3ca0876f4899f8fd75623c398e933</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27915,27916</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29187338$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Aparicio, José L</creatorcontrib><creatorcontrib>Ottobre, Macarena</creatorcontrib><creatorcontrib>Duhalde Vega, Maite</creatorcontrib><creatorcontrib>Coutelier, Jean-Paul</creatorcontrib><creatorcontrib>Van Snick, Jacques</creatorcontrib><creatorcontrib>Retegui, Lilia A</creatorcontrib><title>Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection</title><title>European cytokine network</title><addtitle>Eur Cytokine Netw</addtitle><description>Mice infected with mouse hepatitis virus A59 (MHV-A59) develop hepatitis and autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH), a fact closely related to the release of alarmins such as uric acid and/or high-mobility group box protein 1 (HMGB1). We studied the effect of neutralizing monoclonal antibodies (MAb) against IL-17A in our model of mouse MHV-A59-infection. MAb anti-IL-17F and anti-IFNγ were used to complement the study. Results showed that transaminase levels markedly decreased in MHV-A59-infected mice treated with MAb anti-IL-17A whereas plasmatic Ig concentration sharply increased. Conversely, MAb anti-IL-17F enhanced transaminase liberation and did not affect Ig levels. Serum IFNγ was detected in mice infected with MHV-A59 and its concentration increased after MAb anti-IL-17A administration. Besides, MAb anti-IFNγ greatly augmented transaminase plasmatic levels. IL-17A neutralization did not affect MHV-A59-induction of HMGB1 liberation and slightly augmented plasmatic uric acid concentration. However, mice treated with the MAb failed to produce autoAb to FAH. The above results suggest a reciprocal regulation of Th1 and Th17 cells acting on the different MHV-A59 effects. In addition, it is proposed that IL-17A is involved in alarmins adjuvant effects leading to autoAb expression.</description><subject>Animals</subject><subject>Autoantibodies</subject><subject>Autoantibodies - immunology</subject><subject>Cell Differentiation - physiology</subject><subject>Female</subject><subject>Fumarylacetoacetase</subject><subject>Helper cells</subject><subject>Hepatitis</subject><subject>HMGB1 protein</subject><subject>Hydrolases - metabolism</subject><subject>Immunoglobulins</subject><subject>Interleukin-17 - metabolism</subject><subject>Kidney - metabolism</subject><subject>Kidneys</subject><subject>Liver</subject><subject>Liver - metabolism</subject><subject>Lymphocytes T</subject><subject>Mice</subject><subject>Monoclonal antibodies</subject><subject>Murine hepatitis virus - immunology</subject><subject>Murine hepatitis virus - metabolism</subject><subject>Murine hepatitis virus - pathogenicity</subject><subject>Transaminase</subject><subject>Uric acid</subject><subject>γ-Interferon</subject><issn>1148-5493</issn><issn>1952-4005</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkc1rGzEQxUVpaUKaY69F0Et8WFdaSSvNJWCM8wEOvSS9qlqtFCu1tY60G2j_-miJE1IYmGH0481DD6GvlMxpo_gPZ-O8JlTOCQP4gI4piLrihIiPZaZcVYIDO0KnOYeW1FIQISR8Rkc1UCUZU8fo98p7Z4eMe49DHFzauvFPiJjKBT67Xlelz3B045DMNvwzQ-gjLrUbU4gOb9y-rIaQ8VNIY8ZnN1e_qoWAWdGaZAv9BX3yZpvd6aGfoLuL1e3yqlr_vLxeLtaV5YIPVau6VnivDBVAlOEgOg-NNFK1FnxjAUzHrCFKNp4rAK98J0VTM8tAOWDsBJ2_6O7Hduc66-JkWe9T2Jn0V_cm6P9fYtjo-_5JSwJQM14Evh8EUv84ujzoh35MsXjWFMqphpTfLVT1QtnU55ycf7tAiZ4y0SUTPWWip0wK_-29rTf6NQH2DIwyhxw</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Aparicio, José L</creator><creator>Ottobre, Macarena</creator><creator>Duhalde Vega, Maite</creator><creator>Coutelier, Jean-Paul</creator><creator>Van Snick, Jacques</creator><creator>Retegui, Lilia A</creator><general>Springer Nature B.V</general><general>John Libbey Eurotext</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>5PM</scope></search><sort><creationdate>20170901</creationdate><title>Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection</title><author>Aparicio, José L ; Ottobre, Macarena ; Duhalde Vega, Maite ; Coutelier, Jean-Paul ; Van Snick, Jacques ; Retegui, Lilia A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c454t-b8db5ff8a15908a495df967a78bc9f6c99ad3ca0876f4899f8fd75623c398e933</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Autoantibodies</topic><topic>Autoantibodies - immunology</topic><topic>Cell Differentiation - physiology</topic><topic>Female</topic><topic>Fumarylacetoacetase</topic><topic>Helper cells</topic><topic>Hepatitis</topic><topic>HMGB1 protein</topic><topic>Hydrolases - metabolism</topic><topic>Immunoglobulins</topic><topic>Interleukin-17 - metabolism</topic><topic>Kidney - metabolism</topic><topic>Kidneys</topic><topic>Liver</topic><topic>Liver - metabolism</topic><topic>Lymphocytes T</topic><topic>Mice</topic><topic>Monoclonal antibodies</topic><topic>Murine hepatitis virus - immunology</topic><topic>Murine hepatitis virus - metabolism</topic><topic>Murine hepatitis virus - pathogenicity</topic><topic>Transaminase</topic><topic>Uric acid</topic><topic>γ-Interferon</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aparicio, José L</creatorcontrib><creatorcontrib>Ottobre, Macarena</creatorcontrib><creatorcontrib>Duhalde Vega, Maite</creatorcontrib><creatorcontrib>Coutelier, Jean-Paul</creatorcontrib><creatorcontrib>Van Snick, Jacques</creatorcontrib><creatorcontrib>Retegui, Lilia A</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>European cytokine network</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aparicio, José L</au><au>Ottobre, Macarena</au><au>Duhalde Vega, Maite</au><au>Coutelier, Jean-Paul</au><au>Van Snick, Jacques</au><au>Retegui, Lilia A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection</atitle><jtitle>European cytokine network</jtitle><addtitle>Eur Cytokine Netw</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>28</volume><issue>3</issue><spage>111</spage><epage>119</epage><pages>111-119</pages><issn>1148-5493</issn><eissn>1952-4005</eissn><abstract>Mice infected with mouse hepatitis virus A59 (MHV-A59) develop hepatitis and autoantibodies (autoAb) to liver and kidney fumarylacetoacetate hydrolase (FAH), a fact closely related to the release of alarmins such as uric acid and/or high-mobility group box protein 1 (HMGB1). We studied the effect of neutralizing monoclonal antibodies (MAb) against IL-17A in our model of mouse MHV-A59-infection. MAb anti-IL-17F and anti-IFNγ were used to complement the study. Results showed that transaminase levels markedly decreased in MHV-A59-infected mice treated with MAb anti-IL-17A whereas plasmatic Ig concentration sharply increased. Conversely, MAb anti-IL-17F enhanced transaminase liberation and did not affect Ig levels. Serum IFNγ was detected in mice infected with MHV-A59 and its concentration increased after MAb anti-IL-17A administration. Besides, MAb anti-IFNγ greatly augmented transaminase plasmatic levels. IL-17A neutralization did not affect MHV-A59-induction of HMGB1 liberation and slightly augmented plasmatic uric acid concentration. However, mice treated with the MAb failed to produce autoAb to FAH. The above results suggest a reciprocal regulation of Th1 and Th17 cells acting on the different MHV-A59 effects. 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| subjects | Animals Autoantibodies Autoantibodies - immunology Cell Differentiation - physiology Female Fumarylacetoacetase Helper cells Hepatitis HMGB1 protein Hydrolases - metabolism Immunoglobulins Interleukin-17 - metabolism Kidney - metabolism Kidneys Liver Liver - metabolism Lymphocytes T Mice Monoclonal antibodies Murine hepatitis virus - immunology Murine hepatitis virus - metabolism Murine hepatitis virus - pathogenicity Transaminase Uric acid γ-Interferon |
| title | Effects of interleukin 17A (IL-17A) neutralization on murine hepatitis virus (MHV-A59) infection |
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