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. 2017 May 2;127(6):2339–2352. doi: 10.1172/JCI92217

Figure 7. Phospholipid and cholesterol species, which preferentially accumulate in the skin of hCD1Tg HJ1Tg Apoe–/– mice, can activate HJ1 T cells.

Figure 7

Total lipid was extracted from skin and liver tissues of mice, weighed, and analyzed by mass spectrometry and gas chromatography. (A) Comparison of phospholipid accumulation in the skin of diseased hCD1Tg HJ1Tg Apoe–/– and healthy hCD1Tg HJ1Tg Apoe+/+ mice. (B) Ratio of phospholipids from diseased over healthy mice in the skin and liver. PC, phosphatidylcholine; SM, sphingomyelin; DSM, dihydro-sphingomyelin; ePC, ether-linked phosphatidylcholine; PS, phosphatidylserine; PI, phosphatidylinositol; ePE, ether-linked phosphatidylethanolamine; ePS, ether-linked phosphatidylserine; PA, phosphatidic acid. (C) Comparison of apolar lipid accumulation in the skin of diseased hCD1Tg HJ1Tg Apoe–/– and healthy hCD1Tg HJ1Tg Apoe+/+ mice. (D) Ratio of apolar lipids from diseased over healthy mice in the skin and liver (n = 3). (E) Polar lipid extract (PL), cholesterol (Chol), and fatty acid mixtures (FA1 and FA2) were loaded onto CD1b protein and incubated with HJ1 T cell hybridoma for 24 hours. IL-2 in the supernatant was measured by ELISA. (F) CD1b-autoreactive human T cell clones were stained with mock-loaded CD1b tetramers or PG- or PE-loaded CD1b tetramers. Data are representative of at least 3 experiments. ***P < 0.005; **P < 0.01; *P < 0.05, Student’s t test.