MALT1 promotes the antibacterial immune response by activating NF-κB signaling and enhancing hemocyte phagocytosis in the Chinese mitten crab

Mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT1), a scaffold protein, plays a pivotal role in the NF-κB pathway downstream of T-cell receptors (TCRs) and B-cell receptors (BCRs). As a key signaling hub, MALT1 integrates various pathways, making it essential for both innate and adaptive immunity. However, its role in the antibacterial immune responses of crustaceans remains unclear. Here, we characterized MALT1 from the Chinese mitten crab (Eriocheir sinensis), denoted as EsMALT1, and compared its sequence and domain conservation with MALT1 from other species. Furthermore, Vibrio parahaemolyticus infection upregulated EsMALT1 expression markedly. Knockdown of EsMALT1 in hemocytes inhibits the translocation of the NF-κB-like transcription factors EsRelish and EsDorsal from the cytoplasm to the nucleus in response to Vibrio parahaemolyticus stimulation, thereby reducing the expression of the antimicrobial peptides anti-lipopolysaccharide factor (ALF), and Crustins. At the cellular level, silencing of EsMALT1 expression significantly inhibited the phagocytic capacity of crab hemocytes against Vibrio parahaemolyticus. In vivo, silencing of EsMALT1 rendered crabs susceptible to bacterial infection and impaired their bacterial clearance. In conclusion, EsMALT1 promotes both humoral and cellular immunity in E. sinensis, making it essential for the induction of antibacterial immune responses.