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. 2012 Jul 16;109(31):12698–12703. doi: 10.1073/pnas.1207219109

Fig. 4.

Fig. 4.

MHC II−/− CD8 T cells induced severe colitis and CHS. (A and B) 1 × 106 naive Thy1.1 WT and MHC II KO CD8 T cells were transferred into TCR-β−/− recipients. (A) Body weight was monitored weekly and is presented as percentage of the initial weight at day 0. (B) Lamina propria cells were isolated at 5 wk posttransfer, and cytokine expression was analyzed by intracellular cytokine staining. Total IFN-γ– and IL-17A–producing Thy1.1 CD8 T cells were enumerated. *P < 0.05. (C) WT, CD4−/−, and MHC II−/− mice were sensitized with DNFB as described in Materials and Methods. Draining LN CD8 T cells were isolated on day 5. Then 1 × 107 cells were transferred into naïve WT or MHC II−/− recipients, and the recipients were subsequently challenged on each side of both ears with DNFB. After 16 h, ear swelling was measured. Each symbol represents an individually tested mouse. (D) WT 2C or MHC II−/− 2C TCR Tg CD8 T cells were transferred into Rag−/− mice and then reisolated from the recipients at 7 d posttransfer. An ex vivo killing assay was performed using differentially CFSE-labeled target or control cells. (E) Surface and intracellular LAG-3 expression of WT (black) and MHC II−/− (red) was measured at 7 d posttransfer into Rag−/− mice. (F) WT and MHC II−/− CD8 T cells were transferred into TCR-βδ−/− mice that had been injected with rat IgG or anti–LAG-3 mAb.