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 plays vital role in regulating immune cell polarization, differentiation and effector functions. In this study, we provide evidence low pH impaired the function CD4+ T cells response to TCR non-TCR stimulation. Specifically, or hydrochloric treatment significantly decreased IL-2 IFN-γ production as well CD25/CD69 expression. Furthermore, although MCT1 required for suppression CD25 CD69 expression by acid, using pharmacological inhibition genetic deletion, demonstrated it dispensable acid-mediated production.