MGL1 Receptor Plays a Key Role in the Control of T. cruzi Infection by Increasing Macrophage Activation through Modulation of ERK1/2, c-Jun, NF-κB and NLRP3 Pathways.

摘要: Macrophage galactose-C type lectin (MGL)1 receptor is involved in the recognition of Trypanosoma cruzi (T. cruzi) parasites and important for modulation innate adaptive immune responses. However, mechanism by which MGL1 promotes resistance to T. remains unclear. Here, we show that knockout macrophages (MGL1−/− Mφ) infected vitro with were heavily parasitized showed decreased levels reactive oxygen species (ROS), nitric oxide (NO), IL-12 TNF-α compared wild-type (WT Mφ). MGL1−/− Mφ stimulated antigen (TcAg) low expression TLR-2, TLR-4 MHC-II, resulted deficient splenic cell activation similar co-cultured WT Mφ. Importantly, p-ERK1/2, p-c-Jun p-NF-κB p65 significantly reduced exposed TcAg. Similarly, procaspase 1, caspase 1 NLRP3 inflammasome also displayed a was associated IL-β production. Our data reveal previously unappreciated role through ERK1/2, c-Jun, NF-κB signaling pathways, development protective immunity against experimental infection.