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These subpopulations are determined by the signaling patterns they receive during their initial interaction with the antigen ( Gln deficiency completely eliminated the proliferation of human CD4 + T cells, and inhibition of GLS reduced the proliferation index of human CD4 + T cells during the process of CD3/CD28 signaling activation ( Figure 2 ) ( + T cells into Th17 cells is severely impaired in glutamine-free medium, but Treg cell formation is normal and even appears to be enhanced in expression ( -/- T cells into Th17 cells ( via nucleotide synthesis and the nitrogen-derived action of -KG ( Figure 2 ) ( + Th cells and led to a reduction in IL-17A expression in T cells by more than half ( Figure 2 ) ( Figure 2 ) ( Figure 2 ) ( + T cells that depend on CD3/CD28 signaling promote GLS expression ( + T cells in both of normoxia and hypoxia ( + T cells under this conditions ( + T cells ( Figure 2 Inhibition of GLS leads to increased intracellular Gln, decreased Glu, and decreased intracellular levels of a-KG ( Figure 2 ) ( in vivo , impairs Th1 induction, and attenuates inflammatory T-cell responses ( + T cell proliferation and cytokine production by directly binding to the GAC outside the active site compared to BPTES ( It is increasingly evident that Gln is an immunomodulatory nutrient with multiple biological capabilities and metabolic pathways that are crucial in determining the function of different immune subgroups, especially Th17 cells