Thus, inhibition of IDO1 activity did not significantly alter immunomodulatory properties of TLR-2-primed Gal-3-/-DCs, suggesting that Gal-3 and IDO1 are members of the same TLR-2-initiated signaling pathway which was responsible for nephroprotective and immunosuppressive effects of TLR-2-primed renal DCs in attenuation of CDDP-induced AKI. The gene discussed is TLR2; the disease is acute kidney injury.