Cutting Edge: TLR2-Mediated Proinflammatory Cytokine and Chemokine Production by Microglial Cells in Response to Herpes Simplex Virus
Recent studies indicate that TLRs are critical in generating innate immune responses during infection with HSV-1. In this study, we investigated the role of TLR2 signaling in regulating the production of neuroimmune mediators by examining cytokine and chemokine expression using primary microglial ce...
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Veröffentlicht in: | The Journal of immunology (1950) 2005-10, Vol.175 (7), p.4189-4193 |
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creator | Aravalli, Rajagopal N Hu, Shuxian Rowen, Timothy N Palmquist, Joseph M Lokensgard, James R |
description | Recent studies indicate that TLRs are critical in generating innate immune responses during infection with HSV-1. In this study, we investigated the role of TLR2 signaling in regulating the production of neuroimmune mediators by examining cytokine and chemokine expression using primary microglial cells obtained from TLR2-/- as well as wild-type mice. Data presented here demonstrate that TLR2 signaling is required for the production of proinflammatory cytokines and chemokines: TNF-alpha, IL-1beta, IL-6, IL-12, CCL7, CCL8, CCL9, CXCL1, CXCL2, CXCL4, and CXCL5. CXCL9 and CXCL10 were also induced by HSV, but their production was not dependent upon TLR2 signaling. Because TLR2-/- mice display significantly reduced mortality and diminished neuroinflammation in response to brain infection with HSV, the TLR2-dependent cytokines identified here might function as key players influencing viral neuropathogenesis. |
doi_str_mv | 10.4049/jimmunol.175.7.4189 |
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In this study, we investigated the role of TLR2 signaling in regulating the production of neuroimmune mediators by examining cytokine and chemokine expression using primary microglial cells obtained from TLR2-/- as well as wild-type mice. Data presented here demonstrate that TLR2 signaling is required for the production of proinflammatory cytokines and chemokines: TNF-alpha, IL-1beta, IL-6, IL-12, CCL7, CCL8, CCL9, CXCL1, CXCL2, CXCL4, and CXCL5. CXCL9 and CXCL10 were also induced by HSV, but their production was not dependent upon TLR2 signaling. Because TLR2-/- mice display significantly reduced mortality and diminished neuroinflammation in response to brain infection with HSV, the TLR2-dependent cytokines identified here might function as key players influencing viral neuropathogenesis.</description><subject>Animals</subject><subject>Chemokines - metabolism</subject><subject>Gene Expression Regulation, Viral - immunology</subject><subject>Herpes Simplex - immunology</subject><subject>Herpes Simplex - metabolism</subject><subject>Herpesvirus 1, Human - immunology</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Microglia - immunology</subject><subject>Microglia - metabolism</subject><subject>Microglia - virology</subject><subject>Toll-Like Receptor 2 - genetics</subject><subject>Toll-Like Receptor 2 - physiology</subject><issn>0022-1767</issn><issn>1550-6606</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpNkNuKFDEQhoMo7rj6BILkSq96TPqQTnsnzeoKsyjr6m3IdCozWXNokzTjPIDvbZYZ0avih69-qj6EXlKybkk7vL03zi0-2DXtu3W_bikfHqEV7TpSMUbYY7QipK4r2rP-Aj1L6Z4QwkjdPkUXlNG-J12_Qr_HJWfjd_hK7eAdvtvc1tUNKCMzKPwlBuO1lc7JHOIRj8ccfhgPWHqFxz24UyqYWqZsgsfbI74xUww7a6TFI1ibsPH4FtIcfAKcA76GOEPCX42bLfzC301c0nP0REub4MV5XqJvH67uxutq8_njp_H9ppraluWKyq4hdbcddCPpAIMCrvTANe10PRDZTT3fTnIgvNYNl6xtuJoUL5mVrGXdXKLXp945hp8LpCycSVO5UnoISxKMM1qzhhewOYHll5QiaDFH42Q8CkrEg33x174o9kUvHuyXrVfn-mXrQP3bOesuwJsTsDe7_cFEEMlJawtOxeFw-K_qD_AQkls</recordid><startdate>20051001</startdate><enddate>20051001</enddate><creator>Aravalli, Rajagopal N</creator><creator>Hu, Shuxian</creator><creator>Rowen, Timothy N</creator><creator>Palmquist, Joseph M</creator><creator>Lokensgard, James R</creator><general>Am Assoc Immnol</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>7X8</scope></search><sort><creationdate>20051001</creationdate><title>Cutting Edge: TLR2-Mediated Proinflammatory Cytokine and Chemokine Production by Microglial Cells in Response to Herpes Simplex Virus</title><author>Aravalli, Rajagopal N ; Hu, Shuxian ; Rowen, Timothy N ; Palmquist, Joseph M ; Lokensgard, James R</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c446t-1a53025b9f3a19e9de8df98f15f290a5c78bca9082f38a6438dcd89086f38fa23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Chemokines - metabolism</topic><topic>Gene Expression Regulation, Viral - immunology</topic><topic>Herpes Simplex - immunology</topic><topic>Herpes Simplex - metabolism</topic><topic>Herpesvirus 1, Human - immunology</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Microglia - immunology</topic><topic>Microglia - metabolism</topic><topic>Microglia - virology</topic><topic>Toll-Like Receptor 2 - genetics</topic><topic>Toll-Like Receptor 2 - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Aravalli, Rajagopal N</creatorcontrib><creatorcontrib>Hu, Shuxian</creatorcontrib><creatorcontrib>Rowen, Timothy N</creatorcontrib><creatorcontrib>Palmquist, Joseph M</creatorcontrib><creatorcontrib>Lokensgard, James R</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><jtitle>The Journal of immunology (1950)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Aravalli, Rajagopal N</au><au>Hu, Shuxian</au><au>Rowen, Timothy N</au><au>Palmquist, Joseph M</au><au>Lokensgard, James R</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cutting Edge: TLR2-Mediated Proinflammatory Cytokine and Chemokine Production by Microglial Cells in Response to Herpes Simplex Virus</atitle><jtitle>The Journal of immunology (1950)</jtitle><addtitle>J Immunol</addtitle><date>2005-10-01</date><risdate>2005</risdate><volume>175</volume><issue>7</issue><spage>4189</spage><epage>4193</epage><pages>4189-4193</pages><issn>0022-1767</issn><eissn>1550-6606</eissn><abstract>Recent studies indicate that TLRs are critical in generating innate immune responses during infection with HSV-1. 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subjects | Animals Chemokines - metabolism Gene Expression Regulation, Viral - immunology Herpes Simplex - immunology Herpes Simplex - metabolism Herpesvirus 1, Human - immunology Mice Mice, Inbred C57BL Mice, Knockout Microglia - immunology Microglia - metabolism Microglia - virology Toll-Like Receptor 2 - genetics Toll-Like Receptor 2 - physiology |
title | Cutting Edge: TLR2-Mediated Proinflammatory Cytokine and Chemokine Production by Microglial Cells in Response to Herpes Simplex Virus |
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