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. Author manuscript; available in PMC: 2019 Dec 13.
Published in final edited form as: Cell. 2018 Nov 1;175(7):1780–1795.e19. doi: 10.1016/j.cell.2018.10.001

Figure 2. Th1 and Th17 Cells Differ in Their Use of Glutaminolysis, and GLS Deficiency Is Distinct from Glutamine Deficiency.

Figure 2.

(A) Metabolite fold change from naive in wild-type CD4+ cells maintained in IL-7 (N) or differentiated for 5 days into Th1 (1), Th17 (17), or Treg (R) cells (one-way ANOVA).

(B) Cytokine production from Th1 (top) and Th17 (bottom) differentiated T cells in the presence of glutamine (left), absence of glutamine (middle), or presence of GLS1-inhibitor CB839 (right).

(C) Proliferation of cell trace violet (CTV)-labeled T cells stimulated and differentiated in Th1 or Th17 conditions with (black lines) or without (red lines) glutamine after 3 and 5 days of culture.

(D) Same as in (C), but with vehicle (black lines) or CB839 (green lines).

(E) Foxp3 expression in CD4 T cells activated in Th1- or Th17-skewing conditions in glutamine deficient (red, left) conditions or in the presence of CB839 (green, right).

(F) Heatmap (left) and principle component analysis (right) of metabolites from Th1 and Th17 cells with or without CB839.

Also see Figure S2 and Table S1.