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Furthermore, selective EAAT2 PAM differs considerably from NMDAR antagonists, since its mechanism is to restore glutamate homeostasis by increasing uptake of excessive glutamate, not block glutamatergic transmission, and is expected to be safe and devoid of the dissociative effects observed with NMDAR antagonists

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Just as their functions are unique compared to CD4 + Te cell subsets, Tregs also have distinct metabolic requirements ( Figure 3 b )

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