Slc6a13, also known as GABA transporter 2 (GAT-2), is a member of the neurotransmitter transporter family. It is involved in the transport of γ -amino butyric acid (GABA), with a proposed ion/substrate coupling stoichiometry of 3 Na+: 1 Cl-: 1 GABA [5]. It also has the ability to transport hypotaurine [4]. These transport functions play important roles in processes such as maintaining neurotransmitter homeostasis and cellular antioxidant defense.

In Slc6a13 -deficient (Slc6a13-/-; KO) mice, resistance to Pasteurella multocida infection was observed. This was associated with reduced inflammation, as glycine levels increased in the lungs of KO mice, and glycine supplementation alleviated infection-induced inflammation by blocking inflammasome activation [1]. In another study, Slc6a13 deficiency promoted Th17 cell differentiation in vitro and Th17 responses in a mouse model of intestinal infection and inflammation through activation of GABA-mTOR signaling [2]. Additionally, it was found that GABA transporter 2, encoded by Slc6a13, acts downstream of histone methyltransferase Ezh2 to control axon regeneration in mice [3].

In conclusion, Slc6a13 plays essential roles in immune responses, such as modulating inflammatory responses during bacterial infections and influencing Th17 cell differentiation. It also contributes to axon regeneration. Gene-knockout mouse models have been crucial in revealing these functions, providing insights into potential therapeutic targets for infectious diseases, immune-related disorders, and neural injury repair.