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γ-Aminobutyrate (GAB), the biochemical form of (GABA) γ-aminobutyric acid, participates in shaping physiological processes, including the immune response. How GAB metabolism is controlled to mediate such functions remains elusive. Here we show that GAB is one of the most abundant metabolites in CD4⁺ T helper 17 (T_H17) and induced T regulatory (iT_reg) cells. GAB functions as a bioenergetic and signalling gatekeeper by reciprocally controlling pro-inflammatory T_H17 cell and anti-inflammatory iT_reg cell differentiation through distinct mechanisms. 4-Aminobutyrate aminotransferase (ABAT) funnels GAB into the tricarboxylic acid (TCA) cycle to maximize carbon allocation in promoting T_H17 cell differentiation. By contrast, the absence of ABAT activity in iT_reg cells enables GAB to be exported to the extracellular environment where it acts as an autocrine signalling metabolite that promotes iT_reg cell …