PMID- 23015716
OWN - NLM
STAT- MEDLINE
DCOM- 20130128
LR  - 20211021
IS  - 1098-5514 (Electronic)
IS  - 0022-538X (Print)
IS  - 0022-538X (Linking)
VI  - 86
IP  - 24
DP  - 2012 Dec
TI  - Cross-allele cytotoxic T lymphocyte responses against 2009 pandemic H1N1 
      influenza A virus among HLA-A24 and HLA-A3 supertype-positive individuals.
PG  - 13281-94
LID - 10.1128/JVI.01841-12 [doi]
AB  - Lack of a universal vaccine against all serotypes of influenza A viruses and 
      recent progress on T cell-related vaccines against influenza A virus illuminate 
      the important role of human leukocyte antigen (HLA)-restricted cytotoxic T 
      lymphocytes (CTLs) in anti-influenza virus immunity. However, the diverse HLA 
      alleles among humans complicate virus-specific cellular immunity research, and 
      elucidation of cross-HLA allele T cell responses to influenza virus specificity 
      requires further detailed work. An ideal CTL epitope-based vaccine would cover a 
      broad spectrum of epitope antigens presented by most, if not all, of the HLAs. 
      Here, we evaluated the 2009 pandemic influenza A (H1N1) virus-specific T cell 
      responses among the HLA-A24(+) population using a rationally designed peptide 
      pool during the 2009 pandemic. Unexpectedly, cross-HLA allele T cell responses 
      against the influenza A virus peptides were detected among both HLA-A11(+) and 
      HLA-A24(+) donors. Furthermore, we found cross-responses in the entire HLA-A3 
      supertype population (including HLA-A11, -A31, -A33, and -A30). The cross-allele 
      antigenic peptides within the peptide pool were identified and characterized, and 
      the crystal structures of the major histocompatibility complex (MHC)-peptide 
      complexes were determined. The subsequent HLA-A24-defined cross-allele peptides 
      recognized by the HLA-A11(+) population were shown to mildly bind to the 
      HLA-A*1101 molecule. Together with the structural models, these results partially 
      explain the cross-allele responses. Our findings elucidate the promiscuity of the 
      cross-allele T cell responses against influenza A viruses and are beneficial for 
      the development of a T cell epitope-based vaccine applied in a broader 
      population.
FAU - Liu, Jun
AU  - Liu J
AD  - CAS Key Laboratory of Pathogenic Microbiology and Immunology, Institute of 
      Microbiology, Chinese Academy of Sciences, Beijing, China.
FAU - Zhang, Shihong
AU  - Zhang S
FAU - Tan, Shuguang
AU  - Tan S
FAU - Yi, Yong
AU  - Yi Y
FAU - Wu, Bin
AU  - Wu B
FAU - Cao, Bin
AU  - Cao B
FAU - Zhu, Fengcai
AU  - Zhu F
FAU - Wang, Chen
AU  - Wang C
FAU - Wang, Hua
AU  - Wang H
FAU - Qi, Jianxun
AU  - Qi J
FAU - Gao, George F
AU  - Gao GF
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120926
PL  - United States
TA  - J Virol
JT  - Journal of virology
JID - 0113724
RN  - 0 (HLA-A24 Antigen)
RN  - 0 (HLA-A3 Antigen)
SB  - IM
MH  - Adult
MH  - Aged
MH  - *Alleles
MH  - Amino Acid Sequence
MH  - Cohort Studies
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Female
MH  - HLA-A24 Antigen/chemistry/*immunology
MH  - HLA-A3 Antigen/chemistry/*immunology
MH  - Humans
MH  - Influenza A Virus, H1N1 Subtype/*immunology
MH  - Male
MH  - Middle Aged
MH  - Models, Molecular
MH  - T-Lymphocytes, Cytotoxic/*immunology
PMC - PMC3503122
EDAT- 2012/09/28 06:00
MHDA- 2013/01/29 06:00
PMCR- 2013/06/01
CRDT- 2012/09/28 06:00
PHST- 2012/09/28 06:00 [entrez]
PHST- 2012/09/28 06:00 [pubmed]
PHST- 2013/01/29 06:00 [medline]
PHST- 2013/06/01 00:00 [pmc-release]
AID - JVI.01841-12 [pii]
AID - 01841-12 [pii]
AID - 10.1128/JVI.01841-12 [doi]
PST - ppublish
SO  - J Virol. 2012 Dec;86(24):13281-94. doi: 10.1128/JVI.01841-12. Epub 2012 Sep 26.