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Published Erratum
. 2015 Nov 10;112(45):E6254-6.
doi: 10.1073/pnas.1519135112. Epub 2015 Oct 19.

Correction for Kowalewski et al., HLA ligandome analysis identifies the underlying specificities of spontaneous antileukemia immune responses in chronic lymphocytic leukemia (CLL)

No authors listed
Published Erratum

Correction for Kowalewski et al., HLA ligandome analysis identifies the underlying specificities of spontaneous antileukemia immune responses in chronic lymphocytic leukemia (CLL)

No authors listed. Proc Natl Acad Sci U S A. .
No abstract available

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Figures

Fig. 4.
Fig. 4.
LiTAAs are specifically recognized by CLL patient immune responses. (A) HLA class I LiTAAs and corresponding LiTAPs (3 HLA-A*03, 5 HLA-A*02, 6 HLA-B*07) functionally evaluated in IFNγ ELISPOT assays. Absolute numbers and frequencies of peptide-specific immune recognition by CLL patient PBMC are summarized in the right hand column. (B) Example of A*03 LiTAPs evaluated in ELISPOT using HV PBMC as a control. An EBV epitope mix containing five frequently recognized peptides [BRLF109–117 YVLDHLIVV (A*02), EBNA3471–479 RLRAEAQVK (A*03), EBNA3247–255 RPPIFIRRL (B*07), BZLF1190–197 RAKFKQLL (B*08), EBNA6162–171 AEGGVGWRHW (B*44)] was used as positive control, HIV GAG18–26 A*03 peptide KIRLRPGGK served as negative control. (C) Example of ELISPOT assays using HLA-A*03 LiTAPs (n = 3) on PBMC of three different CLL patients. Results are shown for immunoreactive LiTAPs. EBV epitope mix served as positive control, HIV GAG18–26 A*03 peptide as negative control. (D) Example of HLA-A*03 benign tissue-derived LiBAPs (n = 3) tested on CLL patient PBMC as internal control for the target selection strategy. EBV epitope mix served as positive control, HIV GAG18–26 A*03 peptide as negative control. (E) Scatterplot of the allele-adjusted frequencies of LiTAP presentation in CLL ligandomes (as detected by MS) and the corresponding allele-adjusted frequencies of immune recognition by CLL patient PBMC in IFNγ ELISPOT. Data points are shown for the 14 of 15 LiTAPs showing immune recognition. HV, healthy volunteer; LiBAP, ligandome-defined benign tissue-associated peptide; LiTAP, ligandome-defined tumor-associated peptide; MS, mass spectrometry; neg., negative; pos., positive; UPN, uniform patient number.
Fig. 5.
Fig. 5.
Identification of additional/synergistic HLA class II LiTAAs and LiTAPs. (A) Overlap of HLA class II ligand source proteins of primary CLL samples (n = 20) and HV PBMC (n = 13). (B) Comparative profiling of HLA class II ligand source proteins based on the frequency of HLA restricted representation in CLL and HV PBMC ligandomes. Frequencies [%] of CLL patients/HVs positive for HLA restricted presentation of the respective source protein (x axis) are indicated on the y axis. The box on the left highlights the subset of source proteins showing CLL-exclusive representation in >20% of patients (LiTAAs, ligandome-defined tumor-associated antigens). (C) HLA class II LiTAAs and corresponding LiTAPs (n = 6) functionally evaluated in IFNγ ELISPOT assays. Absolute numbers and frequencies of peptide-specific immune recognition by CLL patient PBMC are summarized in the right column. (D) Example of HLA class II LiTAPs evaluated in ELISPOT using HV PBMC as a control. PHA was used as positive control. FLNA1669–1683 HLA-DR peptide (ETVITVDTKAAGKGK) served as negative control. (E) Example of ELISPOT assays using HLA class II LiTAPs (n = 6) on PBMC of three different CLL patients. Results are shown for immunoreactive LiTAPs. PHA was used as positive control, FLNA1669–1683 HLA-DR peptide served as negative control. (F) Overlap analysis of CLL-exclusive HLA class I and HLA class II ligand source proteins for shared/synergistic vaccine targets. (G) Heatmap analysis of the 132 shared HLA class I/II LiTAAs identified in D. The two source proteins showing representation in ≥20% of both, HLA class I and II CLL patient ligandomes are specified.
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