By using complementary in vitro and in vivo approaches we demonstrated that genetic deletion as well as pharmacological inhibition of Gal-3 significantly impaired capacity of TLR-2-primed renal DCs to express IDO1 and produce immunosuppressive KYN which resulted in significantly reduced presence of renal-infiltrated Tregs and notably aggravated CDDP-induced AKI. The gene discussed is IDO1; the disease is acute kidney injury.