scRNA-seq of WT and TGF-βRII–deficient P14 cells from chronically infected mice. (A) Congenically marked WT and TGF-βRII–deficient (KO) P14 CD8 T cells were cotransferred into naive mice treated with anti-CD4 depleting antibody GK1.5, followed by LCMV clone 13 infection. WT and KO P14 cells were sorted from spleen on D30 p.i. for scRNA-seq. (B) UMAP analyses identified three distinct clusters for both WT and KO P14 cells: stem-like, transitory, and exhausted. (C) An overlay of WT (black) and KO (red) UMAP analyses. (D) UMAP plots showing the expression of selected genes. (E) The frequencies of WT and KO P14 cells in the stem, transitory, and exhausted clusters, with two subclusters identified within the transitory cluster. The green dotted line circles the subcluster at possible pre-exhaustion state.
Figure 4.

scRNA-seq of WT and TGF-βRII–deficient P14 cells from chronically infected mice. (A) Congenically marked WT and TGF-βRII–deficient (KO) P14 CD8 T cells were cotransferred into naive mice treated with anti-CD4 depleting antibody GK1.5, followed by LCMV clone 13 infection. WT and KO P14 cells were sorted from spleen on D30 p.i. for scRNA-seq. (B) UMAP analyses identified three distinct clusters for both WT and KO P14 cells: stem-like, transitory, and exhausted. (C) An overlay of WT (black) and KO (red) UMAP analyses. (D) UMAP plots showing the expression of selected genes. (E) The frequencies of WT and KO P14 cells in the stem, transitory, and exhausted clusters, with two subclusters identified within the transitory cluster. The green dotted line circles the subcluster at possible pre-exhaustion state.

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