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These studies suggest that GLP-1RA may inhibit TCR signaling in a GLP-1R-dependent manner, thereby reducing systemic and intestinal inflammation induced by CD8 + T cells and other factors (anti-CD3 induction) (99)

GLP-1RAs, such as lixisenatide, not only rely on -cell function and glucagon suppression, but also assist to lower glucose by other (insulin-independent) mechanisms such as delayed gastric emptying, underlying the clinical utility of GLP-1RAs as adjuvant therapy to basal insulin in longstanding T2DM [14]