Xu, Q., J. Lee, E. Jankowska-Gan, J. Schultz, D. A. Roennburg, L. D. Haynes, S. Kusaka, H. W. Sollinger, S. J. Knechtle, A. M. VanBuskirk, J. R. Torrealba, and W. J. Burlingham. 2007. Human CD4+CD25low adaptive T regulatory cells suppress delayed-type hypersensitivity during transplant tolerance. J. Immunol. 178: 3983–3995.
The last name of the fifth author was misspelled. The correct name is Drew A. Roenneburg.
In Table I, “off insulin” in footnote b and “ceased insulin” in footnote f should be “off immunosuppression.” The corrected footnotes are shown below.
b Kidney transplant from a deceased donor in 1993 for reflux nephropathy. Off immunosuppression 1995; clinical course described as patient DS elsewhere (25) and in Fig. 3.
f Kidney transplant from a deceased donor in 1986 for chronic glomerulonephritis; off immunosuppression in 2003 due to renal carcinoma in native kidney that was removed in 2004. Current serum creatinine is 1.1 mg/dl.
In Table II, under “Peptide” in the middle column, the labels to the peptides “allo” and “self” are transposed. The corrected table is shown below.
HLA-B peptide sequences
| HLA-B Ag . | Peptide . | Amino Acid Sequences . |
|---|---|---|
| B*1501 | p106 (p106–123) allo | NH2-DGRLLRGHDQSAYDGKDY-COOH |
| B*1501 | p149 (p149–166) allo | NH2-AAREAEQWRAYLEGLCVE-COOH |
| B*1501; B*5701 | p37-MA (p37–54)a allo | NH2-DSDAASPRMAPRAPWIEQ-COOH |
| p37-TE (p37–54) self | NH2-DSDAASPRTEPRAPWIEQ-COOH | |
| B*0801 | p61-F (p61–77)b allo | NH2-DRNTQIFKTNTQTDRES-COOH |
| p61-C (p61–77) self | NH2-DRNTQICKTNTQTDRES-COOH |
| HLA-B Ag . | Peptide . | Amino Acid Sequences . |
|---|---|---|
| B*1501 | p106 (p106–123) allo | NH2-DGRLLRGHDQSAYDGKDY-COOH |
| B*1501 | p149 (p149–166) allo | NH2-AAREAEQWRAYLEGLCVE-COOH |
| B*1501; B*5701 | p37-MA (p37–54)a allo | NH2-DSDAASPRMAPRAPWIEQ-COOH |
| p37-TE (p37–54) self | NH2-DSDAASPRTEPRAPWIEQ-COOH | |
| B*0801 | p61-F (p61–77)b allo | NH2-DRNTQIFKTNTQTDRES-COOH |
| p61-C (p61–77) self | NH2-DRNTQICKTNTQTDRES-COOH |
For the peptide defined by the region from aa 37 to aa 54 we designated the donor allopeptide p37-MA where ″MA″ refers to the polymorphic residues methionine and alanine at positions 44 and 45 (in boldface type), while the corresponding ″self″ peptide p37-TE has threonine and glutamic acid. The MA polymorphism is found predominantly in only two common Caucasian HLA-B antigens, HLA-B*1501 and HLA-B57, a mismatched HLA-B antigen for patient K2.
The polymorphic phenylalanine (F) amino acid is present at position 67 (in boldface type) in all HLA-B8 family members, while the cysteine (C) amino acid (boldface type) is present in the HLA-B14 of patient K2
In Results, there are several errors as follows. In the last sentence of the paragraph under the heading Nonregulated and regulated PBMC samples contain different proportions of IFN-γ- vs TGF-β1-inducible T cells, “TGF-β1” is missing from “anti-TGF-β1 Ab.” The corrected sentence is shown below.
DTH responses to the control peptide, p37-TE, were negative with or without anti-TGF-β1 Ab (Fig. 5C).
In the first sentence of the first paragraph under the heading CD4+CD25low T cells show variable CD25 expression but retain allopeptide-specific TGF-β1 responsiveness after flow sorting and short-term culture, “CD25low T cells” should be “CD25low TR cells” and “TGF-β1” is missing. In the last sentence of the same paragraph, the word “retained” should be “remained.” The corrected sentences are shown below.
The adoptive transfer data, coupled with the finding that mainly CD25low TR cells were induced to express surface TGF-β1 by allopeptide stimulation in vitro (Fig. 4C), raised the possibility that adaptive TR cells are among the CD4+TGF-β1+ T cells in the graft that showed variable CD25 expression by immunostaining.
However, in cultures with medium alone or peptides, >85% remained negative for CD25 and there was no induction of surface TGF-β1 expression by p37-MA relative to p37-TE.
