HLA class I binding 9mer peptides from influenza A virus induce CD4 T cell responses
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HLA class I binding 9mer peptides from influenza A virus induce CD4 T cell responses. / Wang, Mingjun; Larsen, Mette V; Nielsen, Morten; Harndahl, Mikkel; Justesen, Sune; Dziegiel, Morten H; Buus, Søren; Tang, Sheila T; Lund, Ole; Claesson, Mogens H; Wang, Mingjun; Larsen, Mette V; Nielsen, Morten; Harndahl, Mikkel Nors; Justesen, Sune; Dziegiel, Morten H; Buus, Søren; Tang, Sheila Tuyet; Lund, Ole; Claesson, Mogens Helweg.
I: PLoS ONE, Bind 5, Nr. 5, 01.01.2010, s. e10533.Publikation: Bidrag til tidsskrift › Tidsskriftartikel › Forskning › fagfællebedømt
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T1 - HLA class I binding 9mer peptides from influenza A virus induce CD4 T cell responses
AU - Wang, Mingjun
AU - Larsen, Mette V
AU - Nielsen, Morten
AU - Harndahl, Mikkel
AU - Justesen, Sune
AU - Dziegiel, Morten H
AU - Buus, Søren
AU - Tang, Sheila T
AU - Lund, Ole
AU - Claesson, Mogens H
AU - Wang, Mingjun
AU - Larsen, Mette V
AU - Nielsen, Morten
AU - Harndahl, Mikkel Nors
AU - Justesen, Sune
AU - Dziegiel, Morten H
AU - Buus, Søren
AU - Tang, Sheila Tuyet
AU - Lund, Ole
AU - Claesson, Mogens Helweg
PY - 2010/1/1
Y1 - 2010/1/1
N2 - BACKGROUND: Identification of human leukocyte antigen class I (HLA-I) restricted cytotoxic T cell (CTL) epitopes from influenza virus is of importance for the development of new effective peptide-based vaccines. METHODOLOGY/PRINCIPAL FINDINGS: In the present work, bioinformatics was used to predict 9mer peptides derived from available influenza A viral proteins with binding affinity for at least one of the 12 HLA-I supertypes. The predicted peptides were then selected in a way that ensured maximal coverage of the available influenza A strains. One hundred and thirty one peptides were synthesized and their binding affinities for the HLA-I supertypes were measured in a biochemical assay. Influenza-specific T cell responses towards the peptides were quantified using IFNgamma ELISPOT assays with peripheral blood mononuclear cells (PBMC) from adult healthy HLA-I typed donors as responder cells. Of the 131 peptides, 21 were found to induce T cell responses in 19 donors. In the ELISPOT assay, five peptides induced responses that could be totally blocked by the pan-specific anti-HLA-I antibody W6/32, whereas 15 peptides induced responses that could be completely blocked in the presence of the pan-specific anti-HLA class II (HLA-II) antibody IVA12. Blocking of HLA-II subtype reactivity revealed that 8 and 6 peptide responses were blocked by anti-HLA-DR and -DP antibodies, respectively. Peptide reactivity of PBMC depleted of CD4(+) or CD8(+) T cells prior to the ELISPOT culture revealed that effectors are either CD4(+) (the majority of reactivities) or CD8(+) T cells, never a mixture of these subsets. Three of the peptides, recognized by CD4(+) T cells showed binding to recombinant DRA1*0101/DRB1*0401 or DRA1*0101/DRB5*0101 molecules in a recently developed biochemical assay. CONCLUSIONS/SIGNIFICANCE: HLA-I binding 9mer influenza virus-derived peptides induce in many cases CD4(+) T cell responses restricted by HLA-II molecules.
AB - BACKGROUND: Identification of human leukocyte antigen class I (HLA-I) restricted cytotoxic T cell (CTL) epitopes from influenza virus is of importance for the development of new effective peptide-based vaccines. METHODOLOGY/PRINCIPAL FINDINGS: In the present work, bioinformatics was used to predict 9mer peptides derived from available influenza A viral proteins with binding affinity for at least one of the 12 HLA-I supertypes. The predicted peptides were then selected in a way that ensured maximal coverage of the available influenza A strains. One hundred and thirty one peptides were synthesized and their binding affinities for the HLA-I supertypes were measured in a biochemical assay. Influenza-specific T cell responses towards the peptides were quantified using IFNgamma ELISPOT assays with peripheral blood mononuclear cells (PBMC) from adult healthy HLA-I typed donors as responder cells. Of the 131 peptides, 21 were found to induce T cell responses in 19 donors. In the ELISPOT assay, five peptides induced responses that could be totally blocked by the pan-specific anti-HLA-I antibody W6/32, whereas 15 peptides induced responses that could be completely blocked in the presence of the pan-specific anti-HLA class II (HLA-II) antibody IVA12. Blocking of HLA-II subtype reactivity revealed that 8 and 6 peptide responses were blocked by anti-HLA-DR and -DP antibodies, respectively. Peptide reactivity of PBMC depleted of CD4(+) or CD8(+) T cells prior to the ELISPOT culture revealed that effectors are either CD4(+) (the majority of reactivities) or CD8(+) T cells, never a mixture of these subsets. Three of the peptides, recognized by CD4(+) T cells showed binding to recombinant DRA1*0101/DRB1*0401 or DRA1*0101/DRB5*0101 molecules in a recently developed biochemical assay. CONCLUSIONS/SIGNIFICANCE: HLA-I binding 9mer influenza virus-derived peptides induce in many cases CD4(+) T cell responses restricted by HLA-II molecules.
U2 - 10.1371/journal.pone.0010533
DO - 10.1371/journal.pone.0010533
M3 - Journal article
C2 - 20479886
VL - 5
SP - e10533
JO - PLoS ONE
JF - PLoS ONE
SN - 1932-6203
IS - 5
ER -
ID: 20294399