Fig. 2: MHC-I is significantly upregulated on malignant T cells from MF skin lesions.

a Gene set enrichment analysis of overlapping, important tumor (clonal) cell-related genes (N = 48) discovered two important pathways, the MHC class I protein complex and negative regulation of NK cell-mediated immunity. b Gene expression of some of the most important genes (identified via the NN-log-reg method [Fig. 1g]) on their real-time disease stage at follow-up indicated notable escalation in the expression of MHC-I, IFITM1 and IFITM2 as disease progressed. Each dot represented normalized expression of the given marker in a single cell. The larger solid points represented mean normalized expression per patient sample. N = 57 cells from 3 patients were used in stage I-IIA; N = 321 cells from 2 patients were used in stage IIB; N = 814 cells from 8 patients were used in stage III-IVB. Data were presented as mean values +/– SEM of the larger solid points in each stage. For HLA-A and HLA-C, the normalized expression of all transcripts was summed. The p values were calculated using unpaired, two-tailed student’s t test to compare normalized expression at the single-cell level taking the early stage (I-IIA) as reference. n.s., not significant. c Western blot analysis revealing that protein expressions of three classical MHC-I molecules (HLA-A, HLA-B, and HLA-C) were significantly higher on T cells from MF skin lesions (N = 3) compared to healthy skin lesions (N = 3). Conversely, the expression of the non-classical MHC-I molecule (HLA-E) was relatively low on T cells from MF skin lesions. Data were presented as mean values +/– SEM. The p values were calculated using unpaired, two-tailed student’s t test. d Classical MHC-I (HLA-ABC) expression markedly increased on malignant skin T cells (N = 3) compared to bystander T cells in the skin (N = 3) and malignant T cells in the blood (N = 3). Non-classical MHC-I (HLA-E) expression remained low and showed no statistical difference between these samples (N = 3). The p values were calculated using paired, two-tailed student’s t test. Gating strategy is shown in supplementary Fig. 10. e A higher percentage of MHC-I^high T cells was present in malignant T-cell populations from MF skin lesions versus other T-cell populations (representative example of N = 7). f Strong expression of MHC-I on malignant T cells from skin lesions of patients with MF (N = 7) compared with bystander T cells from MF skin lesions (N = 7) or benign T cells from the skin of healthy individuals (N = 5). The expression of MHC-I on malignant T cells in MF skin lesions (N = 7) was also stronger than on malignant and bystander T cells from the blood of patients with L-CTCL (N = 7) and benign blood T cells of healthy individuals (N = 11). Data were presented as mean values +/– SEM. The p values were calculated using unpaired, two-tailed student’s t test. Gating strategy is shown in supplementary Fig. 10. g In addition, the MFI of MHC-I in malignant T cells from MF skin lesions showed significantly greater intensity than in other types of skin tumors, such as basal cell carcinoma (BCC, N = 4), squamous cell carcinoma (SCC, N = 2), cutaneous B-cell lymphoma (CBCL, N = 4) and melanoma (N = 7). Data were presented as mean values +/– SEM. The p values were calculated using unpaired, two-tailed student’s t test. Source data are provided as a Source Data file.