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These mechanisms provide the biological plausibility for cardiorenal benefits observed in GLP-1 RA outcome trials [5, 7, 13]
doi:10.1016/j.path.2009.08.005
The mechanism involves the suppression of pro-inflammatory chemokine (C-C motif) ligand 20 (CCL20), which is of significant importance in the Th17 immune response, as well as IL-33, which is a key cytokine associated with Th2 immune responses [224]
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