PMID- 16451200
OWN - NLM
STAT- MEDLINE
DCOM- 20060331
LR  - 20061115
IS  - 0001-2815 (Print)
IS  - 0001-2815 (Linking)
VI  - 67
IP  - 1
DP  - 2006 Jan
TI  - Inhibitory effects on HLA-DR1-specific T-cell activation by influenza virus 
      haemagglutinin-derived peptides.
PG  - 45-52
AB  - 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. Altered HA308-317 peptides with substitutions of TCR-contact 
      residues may inhibit HLA-DR1/4-specific T-cell activation by blocking the 
      antigen-binding site of HLA-DR1/4 molecules. To evaluate the role of altered 
      HA308-317 peptides in HLA-DR1-restricted T-cell activation, we synthesized three 
      altered HA308-317 peptides. The specific binding of altered HA308-317 peptides to 
      HLA-DR1 molecules was examined using flow cytometry. Effects of altered HA308-317 
      peptides on HLA-DR1-specific T-cell hybridoma were studied by measuring T-cell 
      proliferation and surface expression of CD69 or CD25. The results showed that 
      altered HA308-317 peptides were able to bind to HLA-DR1 molecules and competed 
      with CII263-272 or wildtype HA308-317 peptide. Compared with wildtype CII263-272 
      or HA308-317, altered HA308-317 peptides did not stimulate significant T-cell 
      proliferation and CD69 or CD25 expression. Furthermore, the altered HA308-317 
      peptides inhibited HLA-DR1-specific T-cell activation induced by CII263-272 or 
      wildtype HA308-317 peptide, which may suggest an effective therapeutic strategy 
      in inhibition of HLA-DR1-specific T-cell responses in autoimmunity.
FAU - Li, X
AU  - Li X
AD  - Department of Rheumatology and Immunology, People's Hospital, Beijing University, 
      China.
FAU - Li, R
AU  - Li R
FAU - Li, Z
AU  - Li Z
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - England
TA  - Tissue Antigens
JT  - Tissue antigens
JID - 0331072
RN  - 0 (HLA-DR1 Antigen)
RN  - 0 (HLA-DR4 Antigen)
RN  - 0 (Hemagglutinin Glycoproteins, Influenza Virus)
RN  - 0 (Peptides)
SB  - IM
MH  - Amino Acid Substitution
MH  - Computer Simulation
MH  - HLA-DR1 Antigen/*drug effects/metabolism
MH  - HLA-DR4 Antigen/*drug effects/metabolism
MH  - Hemagglutinin Glycoproteins, Influenza Virus/genetics/*immunology/pharmacology
MH  - Humans
MH  - *Lymphocyte Activation
MH  - Peptides/chemical synthesis/genetics/pharmacology
MH  - T-Lymphocytes/drug effects/*immunology/metabolism
EDAT- 2006/02/03 09:00
MHDA- 2006/04/01 09:00
CRDT- 2006/02/03 09:00
PHST- 2006/02/03 09:00 [pubmed]
PHST- 2006/04/01 09:00 [medline]
PHST- 2006/02/03 09:00 [entrez]
AID - TAN509 [pii]
AID - 10.1111/j.1399-0039.2005.00509.x [doi]
PST - ppublish
SO  - Tissue Antigens. 2006 Jan;67(1):45-52. doi: 10.1111/j.1399-0039.2005.00509.x.