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Blood, Vol. 112, Issue 6, 2369-2380, September 15, 2008
MHC class I–specific inhibitory receptors and their ligands structure diverse human NK-cell repertoires toward a balance of missing self-response
Blood Yawata et al.
112: 2369
Supplemental materials for: Yawata et al
Files in this Data Supplement:
- Figure S1. KIR and HLA class I polymorphisms of the donors (JPG, 134 KB)
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(A) Combinations of KIR haplotype groups (genotypes) are shown on the left. Grey shade indicates presence of the gene, white shows absence. KIR alleles are depicted for KIR2DL2/3, 2DL1, and 3DL1/S1. White triangles for KIR3DP1 indicate the form lacking exon 2, F indicates the full-length form. The number of donors for each genotype is shown on the right; the number of donors analysed to 64-subset resolution is shown in parentheses. (B) HLA-A, -B, and -C alleles in the panel are summarized in panel B. HLA-A and -B alleles with the Bw4 motif, and HLA-C alleles with C1 or C2 motifs are indicated. The number of donors in each grouping is shown in the right column.
- Figure S2. Repertoire deviation from the product rule correlates with the size of the receptor-null subset (JPG, 35.3 KB)
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Deviation from the product rule is shown compared to the amount of receptor-null cells. KIR-KIR co-expression (●), KIR single expression (○), NKG2A-KIR co-expression (▲), NKG2A single expression (△).
- Figure S3. Trend toward higher frequencies of NKG2A-dominant repertoires in group B haplotype donors (JPG, 28.7 KB)
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Frequencies of KIR-dominant (white bars) and NKG2A-dominant (black bars) repertoires in the donor panel are compared between donors homozygous for group A haplotypes (n=29) and donors with group B haplotypes (n=29). The trend towards higher ratios of NKG2A-dominant versus KIR-dominant repertoires in B haplotype donors was not statistically significant.
- Figure S4. The missing-self response of NK cells lacking inhibitory MHC class I receptors varies between human donors (JPG, 107 KB)
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(A) For 58 donors, response against .221 cells of the four NK cell subsets expressing the indicated KIR or NKG2A was compared to the response of the null-receptor subset. In each of the four panels, donors having a MHC class I ligand for the receptor under analysis (●); donors lacking a ligand (○). (B) For the four NK cell subsets the ‘enhanced response,’ due to the presence of cognate ligand, was calculated by subtracting the response of the donor’s receptor-null cells.
- Figure S5. Deviations from the product rule are canceled out separately within the KIR and NKG2A systems (JPG, 27.7 KB)
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The sum of deviation from three sources, KIR single expression, KIR-KIR co-expression and the receptor-null subset, cancel out (▲). The same is observed for the sum of deviation from two sources, NKG2A single expression and NKG2A-KIR co-expression (△). Deviation of KIR single expression (◇) for the 58 donors is ordered on the x axis as in Figure 7A.
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