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Treatment with GABA and GAD65-alum decreases Th1 cytokine responses of polyclonal-stimulated PBMCs. PBMCs from placebo, GABA, and GABA with GAD65-alum treatment groups were collected at 5- and 12 months and stimulated with Dynabeads for 72 h to examine changes in mRNA accumulation by polyclonal stimulation. TaqMan primers and probes specific for proinflammatory genes IFNG (A), IL21 (B), and CXCL10 (C) and anti-inflammatory genes FOXP3 (D) and IL10 (E) are shown. Placebo (n = 18), GABA (n = 24), GABA with GAD65-alum groups (n = 9). Data are shown as mean ± SD. Analyzed by Kruskal–Wallis tests between groups at each time point. * p < 0.05.

Treatment with GABA and GAD65-alum decreases Th1 cytokine responses of polyclonal-stimulated PBMCs. PBMCs from placebo, GABA, and GABA with GAD65-alum treatment groups were collected at 5- and 12 months and stimulated with Dynabeads for 72 h to examine changes in mRNA accumulation by polyclonal stimulation. TaqMan primers and probes specific for proinflammatory genes IFNG (A), IL21 (B), and CXCL10 (C) and anti-inflammatory genes FOXP3 (D) and IL10 (E) are shown. Placebo (n = 18), GABA (n = 24), GABA with GAD65-alum groups (n = 9). Data are shown as mean ± SD. Analyzed by Kruskal–Wallis tests between groups at each time point. * p < 0.05.

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Type 1 diabetes (T1D) is an autoimmune disease culminating in the destruction of insulin-producing pancreatic cells. There is a need for the development of novel antigen-specific strategies to delay cell destruction, including combinatorial strategies that do not elicit systemic immunosuppression. Gamma-aminobutyric acid (GABA) is expressed by immu...