The inhibition of CD4(+) T cell proinflammatory response by lactic acid is independent of monocarboxylate transporter 1

Lactic acid was originally a by-product of glucose metabolism, but many studies have shown that lactic acid plays a vital role in regulating immune cell polarization, differentiation and effector functions. In this study, we provide evidence that lactic acid and low pH impaired the effector function of CD4(+) T cells in response to TCR and non-TCR stimulation. Specifically, lactic acid or hydrochloric acid treatment significantly decreased IL-2 and IFN-gamma production as well as CD25/CD69 expression. Furthermore, although MCT1 was required for the suppression of CD25 and CD69 expression by lactic acid, using pharmacological inhibition and genetic deletion, we demonstrated that it was dispensable for lactic acid-mediated inhibition of IL-2 and IFN-gamma production.