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Article: Superior molecularly altered influenza virus hemagglutinin peptide 308-317 inhibits collagen-induced arthritis by inducing CD4+ treg cell expansion
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TitleSuperior molecularly altered influenza virus hemagglutinin peptide 308-317 inhibits collagen-induced arthritis by inducing CD4+ treg cell expansion
 
AuthorsSun, J3
Li, R3
Guo, J3
Jia, Y3
Sun, X3
Liu, Y3
Li, Y3
Huang, F2
Lu, L1
Li, Z3
 
KeywordsCollagen type 2
Gamma interferon
Influenza virus hemagglutinin[308-317]
Interleukin 10
Interleukin 6
 
Issue Date2012
 
PublisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
 
CitationArthritis & Rheumatism, 2012, v. 64 n. 7, p. 2158-2168 [How to Cite?]
DOI: http://dx.doi.org/10.1002/art.34372
 
AbstractOBJECTIVE: To investigate the inhibitory effect and possible mechanism of a novel influenza virus hemagglutinin 308-317 peptide (altered HA308-317 peptide) in collagen-induced arthritis (CIA). METHODS: CIA was induced in DBA/1 mice by immunization with type II collagen (CII). Altered HA308-317 peptide, wild HA308-317 peptide, wild CII263-272 peptide, and irrelevant peptide were administered intranasally beginning at arthritis onset. Clinical and histologic scores were assessed, and cytokine levels were determined in the serum or in supernatants from splenocytes. Characteristics of T cell subsets in response to different peptides were analyzed both in vivo and in vitro. RESULTS: Intranasal administration of wild CII263-272 peptide, wild HA308-317 peptide, or altered HA308-317 peptide could significantly ameliorate CIA, but altered HA308-317 peptide showed greater therapeutic effects than wild CII263-272 peptide and wild HA308-317 peptide. The effect of altered HA308-317 peptide was associated with a substantial decrease in production of interleukin-17 (IL-17) and interferon-gamma (IFNgamma) and with a marked increase in production of IL-10 and transforming growth factor beta, both in serum and in supernatants from splenocytes treated with altered HA308-317 peptide. Both the number and function of CD4+ Treg cells were significantly up-regulated by altered HA308-317 peptide, with a decreased induction of Th1 cells (CD4+IFNgamma+) and Th17 cells (CD4+IL-17+). Adoptive transfer of CD4+CD25+ T cells from altered HA308-317 peptide-treated mice resulted in greater suppressive capacity in ameliorating CIA severity than did adoptive transfer of CD4+CD25+ T cells from wild HA308-317 peptide-treated, wild CII263-272 peptide-treated, or irrelevant peptide-treated mice. CONCLUSION: Intranasal administration of altered HA308-317 peptide potently suppressed the severity of CIA by increasing the number and function of CD4+ Treg cells, suggesting that altered HA308-317 peptide might be a promising candidate for treatment of rheumatoid arthritis. © 2012, American College of Rheumatology.
 
ISSN0004-3591
2012 Impact Factor: 7.477
2012 SCImago Journal Rankings: 3.012
 
DOIhttp://dx.doi.org/10.1002/art.34372
 
DC FieldValue
dc.contributor.authorSun, J
 
dc.contributor.authorLi, R
 
dc.contributor.authorGuo, J
 
dc.contributor.authorJia, Y
 
dc.contributor.authorSun, X
 
dc.contributor.authorLiu, Y
 
dc.contributor.authorLi, Y
 
dc.contributor.authorHuang, F
 
dc.contributor.authorLu, L
 
dc.contributor.authorLi, Z
 
dc.date.accessioned2012-09-20T08:10:45Z
 
dc.date.available2012-09-20T08:10:45Z
 
dc.date.issued2012
 
dc.description.abstractOBJECTIVE: To investigate the inhibitory effect and possible mechanism of a novel influenza virus hemagglutinin 308-317 peptide (altered HA308-317 peptide) in collagen-induced arthritis (CIA). METHODS: CIA was induced in DBA/1 mice by immunization with type II collagen (CII). Altered HA308-317 peptide, wild HA308-317 peptide, wild CII263-272 peptide, and irrelevant peptide were administered intranasally beginning at arthritis onset. Clinical and histologic scores were assessed, and cytokine levels were determined in the serum or in supernatants from splenocytes. Characteristics of T cell subsets in response to different peptides were analyzed both in vivo and in vitro. RESULTS: Intranasal administration of wild CII263-272 peptide, wild HA308-317 peptide, or altered HA308-317 peptide could significantly ameliorate CIA, but altered HA308-317 peptide showed greater therapeutic effects than wild CII263-272 peptide and wild HA308-317 peptide. The effect of altered HA308-317 peptide was associated with a substantial decrease in production of interleukin-17 (IL-17) and interferon-gamma (IFNgamma) and with a marked increase in production of IL-10 and transforming growth factor beta, both in serum and in supernatants from splenocytes treated with altered HA308-317 peptide. Both the number and function of CD4+ Treg cells were significantly up-regulated by altered HA308-317 peptide, with a decreased induction of Th1 cells (CD4+IFNgamma+) and Th17 cells (CD4+IL-17+). Adoptive transfer of CD4+CD25+ T cells from altered HA308-317 peptide-treated mice resulted in greater suppressive capacity in ameliorating CIA severity than did adoptive transfer of CD4+CD25+ T cells from wild HA308-317 peptide-treated, wild CII263-272 peptide-treated, or irrelevant peptide-treated mice. CONCLUSION: Intranasal administration of altered HA308-317 peptide potently suppressed the severity of CIA by increasing the number and function of CD4+ Treg cells, suggesting that altered HA308-317 peptide might be a promising candidate for treatment of rheumatoid arthritis. © 2012, American College of Rheumatology.
 
dc.description.natureLink_to_subscribed_fulltext
 
dc.identifier.citationArthritis & Rheumatism, 2012, v. 64 n. 7, p. 2158-2168 [How to Cite?]
DOI: http://dx.doi.org/10.1002/art.34372
 
dc.identifier.doihttp://dx.doi.org/10.1002/art.34372
 
dc.identifier.epage2168
 
dc.identifier.hkuros208156
 
dc.identifier.issn0004-3591
2012 Impact Factor: 7.477
2012 SCImago Journal Rankings: 3.012
 
dc.identifier.issue7
 
dc.identifier.openurl
 
dc.identifier.pmid22231228
 
dc.identifier.scopuseid_2-s2.0-84863197516
 
dc.identifier.spage2158
 
dc.identifier.urihttp://hdl.handle.net/10722/164841
 
dc.identifier.volume64
 
dc.languageeng
 
dc.publisherJohn Wiley & Sons, Inc. The Journal's web site is located at http://www.interscience.wiley.com/jpages/0004-3591/
 
dc.publisher.placeUnited States
 
dc.relation.ispartofArthritis & Rheumatism
 
dc.rightsArthritis & Rheumatism. Copyright © John Wiley & Sons, Inc.
 
dc.subject.meshArthritis, Experimental - drug therapy - immunology - pathology
 
dc.subject.meshCell proliferation - drug effects
 
dc.subject.meshHemagglutinins, Viral - pharmacology - therapeutic use
 
dc.subject.meshInterleukin-10 - metabolism
 
dc.subject.meshT-Lymphocytes, Regulatory - drug effects - immunology - pathology
 
dc.subject.meshInterferon-gamma - metabolism
 
dc.subject.meshInterleukin-17 - metabolism
 
dc.subject.meshTransforming growth factor beta - metabolism
 
dc.subjectCollagen type 2
 
dc.subjectGamma interferon
 
dc.subjectInfluenza virus hemagglutinin[308-317]
 
dc.subjectInterleukin 10
 
dc.subjectInterleukin 6
 
dc.titleSuperior molecularly altered influenza virus hemagglutinin peptide 308-317 inhibits collagen-induced arthritis by inducing CD4+ treg cell expansion
 
dc.typeArticle
 
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<contributor.author>Li, R</contributor.author>
<contributor.author>Guo, J</contributor.author>
<contributor.author>Jia, Y</contributor.author>
<contributor.author>Sun, X</contributor.author>
<contributor.author>Liu, Y</contributor.author>
<contributor.author>Li, Y</contributor.author>
<contributor.author>Huang, F</contributor.author>
<contributor.author>Lu, L</contributor.author>
<contributor.author>Li, Z</contributor.author>
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<description.abstract>OBJECTIVE: To investigate the inhibitory effect and possible mechanism of a novel influenza virus hemagglutinin 308-317 peptide (altered HA308-317 peptide) in collagen-induced arthritis (CIA). METHODS: CIA was induced in DBA/1 mice by immunization with type II collagen (CII). Altered HA308-317 peptide, wild HA308-317 peptide, wild CII263-272 peptide, and irrelevant peptide were administered intranasally beginning at arthritis onset. Clinical and histologic scores were assessed, and cytokine levels were determined in the serum or in supernatants from splenocytes. Characteristics of T cell subsets in response to different peptides were analyzed both in vivo and in vitro. RESULTS: Intranasal administration of wild CII263-272 peptide, wild HA308-317 peptide, or altered HA308-317 peptide could significantly ameliorate CIA, but altered HA308-317 peptide showed greater therapeutic effects than wild CII263-272 peptide and wild HA308-317 peptide. The effect of altered HA308-317 peptide was associated with a substantial decrease in production of interleukin-17 (IL-17) and interferon-gamma (IFNgamma) and with a marked increase in production of IL-10 and transforming growth factor beta, both in serum and in supernatants from splenocytes treated with altered HA308-317 peptide. Both the number and function of CD4+ Treg cells were significantly up-regulated by altered HA308-317 peptide, with a decreased induction of Th1 cells (CD4+IFNgamma+) and Th17 cells (CD4+IL-17+). Adoptive transfer of CD4+CD25+ T cells from altered HA308-317 peptide-treated mice resulted in greater suppressive capacity in ameliorating CIA severity than did adoptive transfer of CD4+CD25+ T cells from wild HA308-317 peptide-treated, wild CII263-272 peptide-treated, or irrelevant peptide-treated mice. CONCLUSION: Intranasal administration of altered HA308-317 peptide potently suppressed the severity of CIA by increasing the number and function of CD4+ Treg cells, suggesting that altered HA308-317 peptide might be a promising candidate for treatment of rheumatoid arthritis. &#169; 2012, American College of Rheumatology.</description.abstract>
<language>eng</language>
<publisher>John Wiley &amp; Sons, Inc. The Journal&apos;s web site is located at http://www.interscience.wiley.com/jpages/0004-3591/</publisher>
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<rights>Arthritis &amp; Rheumatism. Copyright &#169; John Wiley &amp; Sons, Inc.</rights>
<subject>Collagen type 2</subject>
<subject>Gamma interferon</subject>
<subject>Influenza virus hemagglutinin[308-317]</subject>
<subject>Interleukin 10</subject>
<subject>Interleukin 6</subject>
<subject.mesh>Arthritis, Experimental - drug therapy - immunology - pathology</subject.mesh>
<subject.mesh>Cell proliferation - drug effects</subject.mesh>
<subject.mesh>Hemagglutinins, Viral - pharmacology - therapeutic use</subject.mesh>
<subject.mesh>Interleukin-10 - metabolism</subject.mesh>
<subject.mesh>T-Lymphocytes, Regulatory - drug effects - immunology - pathology</subject.mesh>
<subject.mesh>Interferon-gamma - metabolism</subject.mesh>
<subject.mesh>Interleukin-17 - metabolism</subject.mesh>
<subject.mesh>Transforming growth factor beta - metabolism</subject.mesh>
<title>Superior molecularly altered influenza virus hemagglutinin peptide 308-317 inhibits collagen-induced arthritis by inducing CD4+ treg cell expansion</title>
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Author Affiliations
  1. The University of Hong Kong
  2. Imperial College London
  3. Peking University