Abstract: C-type lectins are a type of proteins binding to carbohydrates and important pattern recognition receptors in the innate immune system. The classical C-type lectins recognize sugars in Ca²⁺-dependent manners. It is highly acknowledged that Ca²⁺ acts as a second messenger in the cell and participates in a variety of physiological and biochemical process. Heavy metal cadmium can lead to dysregulation of cellular calcium homeostasis and interfere with intracellular Ca²⁺-related information transmission. The aim of this study was to investigate the effects of cadmium stress on the immune responses of two types of lectins, ShLec21 and ShLec23, in the freshwater crab Sinopotamon henanense. The ShLec21 and ShLec23 cDNA were cloned by RACE method, and bioinformatic analysis was carried out. In addition to their constitutive expression in selected tissues, the stimulated expression of the two C-type lectins in hepatopancreas and hemolymph after the treatment of cadmium followed by Aeromonas hydrophila infection were detected. The results showed that ShLec21 cDNA was 863 bp in length that potentinally encoded 152 amino acid residues and ShLec23 cDNA was 681 bp in length that encoded 164 amino acid residues. ShLec21 and ShLec23 clustered into two branches of invertebrates. Both of ShLec21 and ShLec23 were widely expressed in hemolymph, gill, hepatopancreas, intestine, muscle, ovary and testis with highest level in hepatopancreas. Cadmium stress had no significant effect on the expression of ShLec21 and ShLec23 in hepatopancreas and hemolymph. Bacteria A. hydrophila infection significantly down-regulated the expression of ShLec21 (P<0.05) andShLec23 (P<0.01) in the hepatopancreas, and significantly (P<0.05) reduced the expression ofShLec23 in hemolymph. However, in the course of infection with A. hydrophila after cadmium stress, the expression levels of ShLec21 (P<0.05) andShLec23 (P<0.01) were significantly up-regulated in hepatopancreas and hemolymph. The results suggest that cadmium stress could upregulate the expression ofShLec21 and ShLec23 in response to A. hydrophila infection in a certain extent.