Cathelicidin antimicrobial peptide LL-37 augments interferon-β expression and antiviral activity induced by double-stranded RNA in keratinocytes
Summary Background Cathelicidin antimicrobial peptide LL‐37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL‐37 and DNA greatly increases interferon (IFN)‐β through Toll‐like receptor (TLR)9. Howeve...
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| Veröffentlicht in: | British journal of dermatology (1951) 2014-09, Vol.171 (3), p.492-498 |
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| container_title | British journal of dermatology (1951) |
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| creator | Takiguchi, T. Morizane, S. Yamamoto, T. Kajita, A. Ikeda, K. Iwatsuki, K. |
| description | Summary
Background
Cathelicidin antimicrobial peptide LL‐37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL‐37 and DNA greatly increases interferon (IFN)‐β through Toll‐like receptor (TLR)9. However, the effect of LL‐37 on the induction of IFN‐β through TLR3, a sensor of double‐stranded (ds) RNA, in keratinocytes is not well known.
Objectives
To investigate whether LL‐37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs).
Methods
We investigated the production of IFN‐β in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL‐37. To examine the effect of LL‐37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type‐1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL‐37. Immunostaining for TLR3 and LL‐37 was performed using skin samples from HS.
Results
LL‐37 and poly (I:C) synergistically induced the expression of IFN‐β in NHEKs. Furthermore, co‐stimulation with LL‐37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL‐37 alone. LL‐37 enhanced the uptake of FITC‐conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL‐37 is upregulated in HS lesions.
Conclusions
Our findings suggest that LL‐37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
What's already known about this topic?
LL‐37 enhances DNA uptake into intracellular compartments, which leads to Toll‐like receptor (TLR)9‐ and TLR7‐dependent overproduction of interferons (IFNs) in dendritic cells.
In keratinocytes, LL‐37 enhances the responsiveness of TLR9.
LL‐37 modulates poly (I:C)‐induced proinflammatory responses in keratinocytes.
What does this study add?
In keratinocytes, LL‐37 enhances the expression of IFN‐β and antiviral activity induced by poly (I:C). |
| doi_str_mv | 10.1111/bjd.12942 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_journals_2311144364</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>2311144364</sourcerecordid><originalsourceid>FETCH-LOGICAL-c5402-7a58c6ef89d3a6efe11ef3bdb87e78081814f1d603edb8c62f1bdaee164b2aff3</originalsourceid><addsrcrecordid>eNp1kMtu1DAUhi0EokNhwQsgS6xYuPUlcTLLMjCldFQE4rK07PgYPM0kqe20zWPwKn0QnglPp-2u3hzr-Pt_Sx9Crxk9YPkcmrU9YHxe8CdoxoQsCWdCPEUzSmlF6FyKPfQixjWlTNCSPkd7vJCU1SWfob8Lnf5A6xtvfYd1l_zGN6E3Xrd4gCF5C3i1IqLCevy9gS5F7LsEwUHoO_LvBsP1ECBG32_T9rbh0oec1s32lqbM27EBi82EbT-aFkhMIbN59e3sKD_jcwg6-a5vpgTxJXrmdBvh1d3cRz-WH78vPpHVl-OTxdGKNGVBOal0WTcSXD23QucJjIETxpq6gqqmNatZ4ZiVVEDeNZI7ZqwGYLIwXDsn9tHbXe8Q-osRYlLrfgxd_lJxka0WhZBFpt7tqCwlxgBODcFvdJgUo2orX2X56lZ-Zt_cNY5mA_aBvLedgcMdcOVbmB5vUu8_f7ivJLuEjwmuHxI6nCtZiapUv86O1XLJT8uvy59KiP8VoKEQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2311144364</pqid></control><display><type>article</type><title>Cathelicidin antimicrobial peptide LL-37 augments interferon-β expression and antiviral activity induced by double-stranded RNA in keratinocytes</title><source>MEDLINE</source><source>Oxford University Press Journals Current</source><source>Wiley Online Library Journals Frontfile Complete</source><creator>Takiguchi, T. ; Morizane, S. ; Yamamoto, T. ; Kajita, A. ; Ikeda, K. ; Iwatsuki, K.</creator><creatorcontrib>Takiguchi, T. ; Morizane, S. ; Yamamoto, T. ; Kajita, A. ; Ikeda, K. ; Iwatsuki, K.</creatorcontrib><description>Summary
Background
Cathelicidin antimicrobial peptide LL‐37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL‐37 and DNA greatly increases interferon (IFN)‐β through Toll‐like receptor (TLR)9. However, the effect of LL‐37 on the induction of IFN‐β through TLR3, a sensor of double‐stranded (ds) RNA, in keratinocytes is not well known.
Objectives
To investigate whether LL‐37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs).
Methods
We investigated the production of IFN‐β in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL‐37. To examine the effect of LL‐37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type‐1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL‐37. Immunostaining for TLR3 and LL‐37 was performed using skin samples from HS.
Results
LL‐37 and poly (I:C) synergistically induced the expression of IFN‐β in NHEKs. Furthermore, co‐stimulation with LL‐37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL‐37 alone. LL‐37 enhanced the uptake of FITC‐conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL‐37 is upregulated in HS lesions.
Conclusions
Our findings suggest that LL‐37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
What's already known about this topic?
LL‐37 enhances DNA uptake into intracellular compartments, which leads to Toll‐like receptor (TLR)9‐ and TLR7‐dependent overproduction of interferons (IFNs) in dendritic cells.
In keratinocytes, LL‐37 enhances the responsiveness of TLR9.
LL‐37 modulates poly (I:C)‐induced proinflammatory responses in keratinocytes.
What does this study add?
In keratinocytes, LL‐37 enhances the expression of IFN‐β and antiviral activity induced by poly (I:C).</description><identifier>ISSN: 0007-0963</identifier><identifier>EISSN: 1365-2133</identifier><identifier>DOI: 10.1111/bjd.12942</identifier><identifier>PMID: 24601852</identifier><language>eng</language><publisher>England: Blackwell Publishing Ltd</publisher><subject>Antimicrobial peptides ; Antiviral activity ; Antiviral Agents - pharmacokinetics ; Antiviral Agents - pharmacology ; Antiviral drugs ; Cathelicidins - pharmacology ; Cells, Cultured ; Dose-Response Relationship, Drug ; Double-stranded RNA ; Drug Combinations ; Drug Synergism ; Fluorescein isothiocyanate ; Herpes simplex ; Herpes Simplex - drug therapy ; Herpes Simplex - immunology ; Herpesvirus 1, Human - drug effects ; Herpesvirus 1, Human - immunology ; Humans ; Immune response ; Immunity, Innate - drug effects ; Innate immunity ; Interferon ; Interferon Inducers - pharmacokinetics ; Interferon Inducers - pharmacology ; Interferon-beta - biosynthesis ; Keratinocytes ; Keratinocytes - immunology ; Keratinocytes - metabolism ; Keratinocytes - virology ; Peptides ; Plaque assay ; Poly I-C - pharmacokinetics ; Poly I-C - pharmacology ; Polyinosinic:polycytidylic acid ; Ribonucleic acid ; RNA ; RNA, Double-Stranded - physiology ; Signal Transduction - drug effects ; TLR3 protein ; Toll-Like Receptor 3 - drug effects ; Toll-Like Receptor 3 - physiology ; Toll-like receptors ; Up-Regulation ; Viral infections</subject><ispartof>British journal of dermatology (1951), 2014-09, Vol.171 (3), p.492-498</ispartof><rights>2014 British Association of Dermatologists</rights><rights>2014 British Association of Dermatologists.</rights><rights>Copyright © 2014 British Association of Dermatologists</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5402-7a58c6ef89d3a6efe11ef3bdb87e78081814f1d603edb8c62f1bdaee164b2aff3</citedby><cites>FETCH-LOGICAL-c5402-7a58c6ef89d3a6efe11ef3bdb87e78081814f1d603edb8c62f1bdaee164b2aff3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fbjd.12942$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fbjd.12942$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,776,780,1411,27901,27902,45550,45551</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24601852$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Takiguchi, T.</creatorcontrib><creatorcontrib>Morizane, S.</creatorcontrib><creatorcontrib>Yamamoto, T.</creatorcontrib><creatorcontrib>Kajita, A.</creatorcontrib><creatorcontrib>Ikeda, K.</creatorcontrib><creatorcontrib>Iwatsuki, K.</creatorcontrib><title>Cathelicidin antimicrobial peptide LL-37 augments interferon-β expression and antiviral activity induced by double-stranded RNA in keratinocytes</title><title>British journal of dermatology (1951)</title><addtitle>Br J Dermatol</addtitle><description>Summary
Background
Cathelicidin antimicrobial peptide LL‐37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL‐37 and DNA greatly increases interferon (IFN)‐β through Toll‐like receptor (TLR)9. However, the effect of LL‐37 on the induction of IFN‐β through TLR3, a sensor of double‐stranded (ds) RNA, in keratinocytes is not well known.
Objectives
To investigate whether LL‐37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs).
Methods
We investigated the production of IFN‐β in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL‐37. To examine the effect of LL‐37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type‐1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL‐37. Immunostaining for TLR3 and LL‐37 was performed using skin samples from HS.
Results
LL‐37 and poly (I:C) synergistically induced the expression of IFN‐β in NHEKs. Furthermore, co‐stimulation with LL‐37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL‐37 alone. LL‐37 enhanced the uptake of FITC‐conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL‐37 is upregulated in HS lesions.
Conclusions
Our findings suggest that LL‐37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
What's already known about this topic?
LL‐37 enhances DNA uptake into intracellular compartments, which leads to Toll‐like receptor (TLR)9‐ and TLR7‐dependent overproduction of interferons (IFNs) in dendritic cells.
In keratinocytes, LL‐37 enhances the responsiveness of TLR9.
LL‐37 modulates poly (I:C)‐induced proinflammatory responses in keratinocytes.
What does this study add?
In keratinocytes, LL‐37 enhances the expression of IFN‐β and antiviral activity induced by poly (I:C).</description><subject>Antimicrobial peptides</subject><subject>Antiviral activity</subject><subject>Antiviral Agents - pharmacokinetics</subject><subject>Antiviral Agents - pharmacology</subject><subject>Antiviral drugs</subject><subject>Cathelicidins - pharmacology</subject><subject>Cells, Cultured</subject><subject>Dose-Response Relationship, Drug</subject><subject>Double-stranded RNA</subject><subject>Drug Combinations</subject><subject>Drug Synergism</subject><subject>Fluorescein isothiocyanate</subject><subject>Herpes simplex</subject><subject>Herpes Simplex - drug therapy</subject><subject>Herpes Simplex - immunology</subject><subject>Herpesvirus 1, Human - drug effects</subject><subject>Herpesvirus 1, Human - immunology</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunity, Innate - drug effects</subject><subject>Innate immunity</subject><subject>Interferon</subject><subject>Interferon Inducers - pharmacokinetics</subject><subject>Interferon Inducers - pharmacology</subject><subject>Interferon-beta - biosynthesis</subject><subject>Keratinocytes</subject><subject>Keratinocytes - immunology</subject><subject>Keratinocytes - metabolism</subject><subject>Keratinocytes - virology</subject><subject>Peptides</subject><subject>Plaque assay</subject><subject>Poly I-C - pharmacokinetics</subject><subject>Poly I-C - pharmacology</subject><subject>Polyinosinic:polycytidylic acid</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Double-Stranded - physiology</subject><subject>Signal Transduction - drug effects</subject><subject>TLR3 protein</subject><subject>Toll-Like Receptor 3 - drug effects</subject><subject>Toll-Like Receptor 3 - physiology</subject><subject>Toll-like receptors</subject><subject>Up-Regulation</subject><subject>Viral infections</subject><issn>0007-0963</issn><issn>1365-2133</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtu1DAUhi0EokNhwQsgS6xYuPUlcTLLMjCldFQE4rK07PgYPM0kqe20zWPwKn0QnglPp-2u3hzr-Pt_Sx9Crxk9YPkcmrU9YHxe8CdoxoQsCWdCPEUzSmlF6FyKPfQixjWlTNCSPkd7vJCU1SWfob8Lnf5A6xtvfYd1l_zGN6E3Xrd4gCF5C3i1IqLCevy9gS5F7LsEwUHoO_LvBsP1ECBG32_T9rbh0oec1s32lqbM27EBi82EbT-aFkhMIbN59e3sKD_jcwg6-a5vpgTxJXrmdBvh1d3cRz-WH78vPpHVl-OTxdGKNGVBOal0WTcSXD23QucJjIETxpq6gqqmNatZ4ZiVVEDeNZI7ZqwGYLIwXDsn9tHbXe8Q-osRYlLrfgxd_lJxka0WhZBFpt7tqCwlxgBODcFvdJgUo2orX2X56lZ-Zt_cNY5mA_aBvLedgcMdcOVbmB5vUu8_f7ivJLuEjwmuHxI6nCtZiapUv86O1XLJT8uvy59KiP8VoKEQ</recordid><startdate>201409</startdate><enddate>201409</enddate><creator>Takiguchi, T.</creator><creator>Morizane, S.</creator><creator>Yamamoto, T.</creator><creator>Kajita, A.</creator><creator>Ikeda, K.</creator><creator>Iwatsuki, K.</creator><general>Blackwell Publishing Ltd</general><general>Oxford University Press</general><scope>BSCLL</scope><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>H94</scope><scope>K9.</scope><scope>NAPCQ</scope></search><sort><creationdate>201409</creationdate><title>Cathelicidin antimicrobial peptide LL-37 augments interferon-β expression and antiviral activity induced by double-stranded RNA in keratinocytes</title><author>Takiguchi, T. ; Morizane, S. ; Yamamoto, T. ; Kajita, A. ; Ikeda, K. ; Iwatsuki, K.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5402-7a58c6ef89d3a6efe11ef3bdb87e78081814f1d603edb8c62f1bdaee164b2aff3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Antimicrobial peptides</topic><topic>Antiviral activity</topic><topic>Antiviral Agents - pharmacokinetics</topic><topic>Antiviral Agents - pharmacology</topic><topic>Antiviral drugs</topic><topic>Cathelicidins - pharmacology</topic><topic>Cells, Cultured</topic><topic>Dose-Response Relationship, Drug</topic><topic>Double-stranded RNA</topic><topic>Drug Combinations</topic><topic>Drug Synergism</topic><topic>Fluorescein isothiocyanate</topic><topic>Herpes simplex</topic><topic>Herpes Simplex - drug therapy</topic><topic>Herpes Simplex - immunology</topic><topic>Herpesvirus 1, Human - drug effects</topic><topic>Herpesvirus 1, Human - immunology</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunity, Innate - drug effects</topic><topic>Innate immunity</topic><topic>Interferon</topic><topic>Interferon Inducers - pharmacokinetics</topic><topic>Interferon Inducers - pharmacology</topic><topic>Interferon-beta - biosynthesis</topic><topic>Keratinocytes</topic><topic>Keratinocytes - immunology</topic><topic>Keratinocytes - metabolism</topic><topic>Keratinocytes - virology</topic><topic>Peptides</topic><topic>Plaque assay</topic><topic>Poly I-C - pharmacokinetics</topic><topic>Poly I-C - pharmacology</topic><topic>Polyinosinic:polycytidylic acid</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Double-Stranded - physiology</topic><topic>Signal Transduction - drug effects</topic><topic>TLR3 protein</topic><topic>Toll-Like Receptor 3 - drug effects</topic><topic>Toll-Like Receptor 3 - physiology</topic><topic>Toll-like receptors</topic><topic>Up-Regulation</topic><topic>Viral infections</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Takiguchi, T.</creatorcontrib><creatorcontrib>Morizane, S.</creatorcontrib><creatorcontrib>Yamamoto, T.</creatorcontrib><creatorcontrib>Kajita, A.</creatorcontrib><creatorcontrib>Ikeda, K.</creatorcontrib><creatorcontrib>Iwatsuki, K.</creatorcontrib><collection>Istex</collection><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>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><jtitle>British journal of dermatology (1951)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Takiguchi, T.</au><au>Morizane, S.</au><au>Yamamoto, T.</au><au>Kajita, A.</au><au>Ikeda, K.</au><au>Iwatsuki, K.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cathelicidin antimicrobial peptide LL-37 augments interferon-β expression and antiviral activity induced by double-stranded RNA in keratinocytes</atitle><jtitle>British journal of dermatology (1951)</jtitle><addtitle>Br J Dermatol</addtitle><date>2014-09</date><risdate>2014</risdate><volume>171</volume><issue>3</issue><spage>492</spage><epage>498</epage><pages>492-498</pages><issn>0007-0963</issn><eissn>1365-2133</eissn><abstract>Summary
Background
Cathelicidin antimicrobial peptide LL‐37 has the capacity to kill a wide range of microbes and to modify host immunity. Recently, our group observed that the activation of keratinocytes by LL‐37 and DNA greatly increases interferon (IFN)‐β through Toll‐like receptor (TLR)9. However, the effect of LL‐37 on the induction of IFN‐β through TLR3, a sensor of double‐stranded (ds) RNA, in keratinocytes is not well known.
Objectives
To investigate whether LL‐37 could affect TLR3 signalling and antiviral activity in normal human epidermal keratinocytes (NHEKs).
Methods
We investigated the production of IFN‐β in NHEKs stimulated with a TLR3 ligand, poly (I:C), in the presence of LL‐37. To examine the effect of LL‐37 and poly (I:C) on antiviral activity, a virus plaque assay using herpes simplex (HS) virus type‐1 was carried out. The uptake of poly (I:C) conjugated with fluorescein isothiocyanate (FITC) into the keratinocytes was observed in the presence of LL‐37. Immunostaining for TLR3 and LL‐37 was performed using skin samples from HS.
Results
LL‐37 and poly (I:C) synergistically induced the expression of IFN‐β in NHEKs. Furthermore, co‐stimulation with LL‐37 and poly (I:C) significantly decreased the viral plaque numbers compared with poly (I:C) or LL‐37 alone. LL‐37 enhanced the uptake of FITC‐conjugated poly (I:C) into cells. Immunohistochemical analysis demonstrated that the expression of TLR3 and LL‐37 is upregulated in HS lesions.
Conclusions
Our findings suggest that LL‐37 augments the antiviral activity induced by dsRNA in keratinocytes, which may contribute to the innate immune response to cutaneous viral infections such as HS.
What's already known about this topic?
LL‐37 enhances DNA uptake into intracellular compartments, which leads to Toll‐like receptor (TLR)9‐ and TLR7‐dependent overproduction of interferons (IFNs) in dendritic cells.
In keratinocytes, LL‐37 enhances the responsiveness of TLR9.
LL‐37 modulates poly (I:C)‐induced proinflammatory responses in keratinocytes.
What does this study add?
In keratinocytes, LL‐37 enhances the expression of IFN‐β and antiviral activity induced by poly (I:C).</abstract><cop>England</cop><pub>Blackwell Publishing Ltd</pub><pmid>24601852</pmid><doi>10.1111/bjd.12942</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0007-0963 |
| ispartof | British journal of dermatology (1951), 2014-09, Vol.171 (3), p.492-498 |
| issn | 0007-0963 1365-2133 |
| language | eng |
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| source | MEDLINE; Oxford University Press Journals Current; Wiley Online Library Journals Frontfile Complete |
| subjects | Antimicrobial peptides Antiviral activity Antiviral Agents - pharmacokinetics Antiviral Agents - pharmacology Antiviral drugs Cathelicidins - pharmacology Cells, Cultured Dose-Response Relationship, Drug Double-stranded RNA Drug Combinations Drug Synergism Fluorescein isothiocyanate Herpes simplex Herpes Simplex - drug therapy Herpes Simplex - immunology Herpesvirus 1, Human - drug effects Herpesvirus 1, Human - immunology Humans Immune response Immunity, Innate - drug effects Innate immunity Interferon Interferon Inducers - pharmacokinetics Interferon Inducers - pharmacology Interferon-beta - biosynthesis Keratinocytes Keratinocytes - immunology Keratinocytes - metabolism Keratinocytes - virology Peptides Plaque assay Poly I-C - pharmacokinetics Poly I-C - pharmacology Polyinosinic:polycytidylic acid Ribonucleic acid RNA RNA, Double-Stranded - physiology Signal Transduction - drug effects TLR3 protein Toll-Like Receptor 3 - drug effects Toll-Like Receptor 3 - physiology Toll-like receptors Up-Regulation Viral infections |
| title | Cathelicidin antimicrobial peptide LL-37 augments interferon-β expression and antiviral activity induced by double-stranded RNA in keratinocytes |
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