Regulation of Cutaneous Malignancy by T Cells Michael Girardi, David E. Oppenheim, Carrie R. Steele, Julia M. Lewis, Earl Glusac, Renata Filler, Paul Hobby, Brian Sutton, Robert E. Tigelaar, Adrian C. Hayday

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Supplemental Figure 2. (A) Surface representations of (left) Rae-1 modeled on ZAG; (center) the complex between MICA (below) and NKG2d (above in ribbon); and (right) MHC H2Db with bound peptide in green and 2-microglobulin in purple. All three structures are viewed in the same orientation with helix 1 in yellow and 2 in orange. Rae-1 has a stalk region (not shown), which is expected to be part extended and part helical and heavily O-glycosylated in addition to the GPI linkage. (B) Orthogonal views of Rae-1 and MICA, showing the similar distribution of charged residues at the interface. Residues indicated in Rae-1 are D175, E189 (red), R103, and K110 (blue); in MICA, they are D65, D149, D163 (red), R74, and K81 (blue). Figure was generated by INSIGHT.

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Supplemental Figure 3. Expression of Rae-1 and H60 in cell lines. Cell lines are Pam2-12, a keratinocyte line; CMT93, a colorectal carcinoma from C57/BL6 strain; NIH3T3 immortalized embryonic fibroblasts; L-929, a fibroblast-like cell line; J558L, an induced B cell myeloma from Balb/C strain; three thymomas: 4G4, C58, and 34.1; and CTLL2, an IL-2-dependent T cell line. An asterisk denotes that CTLL2 expresses neither Rae-1 nor H60 and did not stain with NKG2d beads.

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