Objective: To study the inhibitory role of altered HA308 - 317 peptides in T cell responses in patients with rheumatoid arthritis (RA).
Methods: Peripheral blood mononuclear cells (PBMC) were obtained from 27 HLA-DRB1 positive RA patients. T cell responses to altered HA308-317 peptides were examined by using (3)H incorporation assay. The level of IL-2 and IFNgamma in the supernatants was identified by an enzyme-linked immunosorbent assay. The CD69 expression on T cell surface was studied by using flow cytometry.
Results: Compared to wild type CII263 - 272 or HA308 - 317, altered HA308 - 317 peptides failed to stimulate T cell proliferation (P < 0.05) and production of IL-2 as well as IFNgamma and resulted in lower expression of CD69 in RA patients (P < 0.05). SI values for T cell coincubated with altered HA308 - 317 peptides and CII263 - 272 or wild type HA308 - 317 were significantly lower than coincubated with CII263 - 272 and wild type HA308 - 317 alone (P < 0.05).
Conclusion: Substitution of TCR-binding residue of HA308 - 317 yielded weak or non-T-cell stimulating peptides, which might be potentially effective in blocking abnormal T cell responses in RA.
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Superior molecularly altered influenza virus hemagglutinin peptide 308-317 inhibits collagen-induced arthritis by inducing CD4+ Treg cell expansion.
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Department of Rheumatology and Immunology, Clinical Immunology Center, Peking University People's Hospital, Beijing, China.
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).
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Altered influenza virus haemagglutinin (HA)-derived peptide is potent therapy for CIA by inducing Th1 to Th2 shift.
Cell Mol Immunol
July 2011
Department of Rheumatology and Immunology, Clinical Immunology Center, Peking University People's Hospital, Beijing, China.
There has been an increase in interest in the use of altered peptides as antigen-specific therapeutic agents in autoimmune diseases. Here we investigated the inhibitory effect and possible mechanism of an altered influenza virus haemagglutinin (HA)-derived peptide in collagen-induced arthritis (CIA). CIA was induced in DBA/1 mice by immunisation with type II collagen (CII).
View Article and Find Full Text PDF[Relationship between HLA-DR4/1 subtypes and T cell response to influenza virus hemagglutinin or anti-HA308-317 antibodies in rheumatoid arthritis].
Zhonghua Yi Xue Za Zhi
July 2008
Teaching-Research Office of Immunology, Dalian University Medical School, Dalian 116622, China.
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Methods: The peripheral blood mononuclear cells (PBMCs) from 70 RA patients were cultured with HA308-317 for 5 days. T cell proliferative responses to HA308-317 were evaluated by [3H] thymidine incorporation assay.
Influenza virus haemagglutinin-derived peptides inhibit T-cell activation induced by HLA-DR4/1 specific peptides in rheumatoid arthritis.
Clin Exp Rheumatol
June 2006
Department of Rheumatology and Immunology, People's Hospital, Beijing University, Beijing, China.
Objective: To investigate whether influenza virus haemagglutinin (HA)-derived altered peptide ligands (APLs) could abrogate T-cell responses to wild type HA308-317 or type II collagen (CII) 263-272 peptides and explore the potential inhibitory effects of the altered HA308-317 peptides on T-cell activation in rheumatoid arthritis (RA).
Methods: Altered HA308-317 peptides containing substitutions of T-cell receptor (TCR)-contact residues were synthesized. Peripheral blood mononuclear cells (PBMC) were obtained from 27 HLA-DR4/1-positive RA patients.
Inhibitory effects on HLA-DR1-specific T-cell activation by influenza virus haemagglutinin-derived peptides.
Tissue Antigens
January 2006
Department of Rheumatology and Immunology, People's Hospital, Beijing University, China.
Collagen (CII) 263-272 peptide, an autoantigen in rheumatoid arthritis, is a specific human leukocyte antigen (HLA)-DR1/4-binding peptide recognized by T-cell receptors (TCR). The affinity of influenza virus haemagglutinin (HA) 306-318 peptide for the antigen-binding groove of HLA-DR1/4 molecules is higher than that of CII263-272. The HLA-DR1/4-binding residues of HA306-318 are located in the region 308-317.
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