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
2011 Impact Factor: 7.866
2011 SCImago Journal Rankings: 0.871
DOIhttp://dx.doi.org/10.1002/art.34372
DC Field
Value
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
2011 Impact Factor: 7.866
2011 SCImago Journal Rankings: 0.871
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
Author Affiliations
  1. The University of Hong Kong
  2. Imperial College London
  3. Peking University