RESUMEN
In response to invading parasites, one of the principal arms of innate immunity is oxidative stress, caused by reactive oxygen species (ROS). However, oxidative stresses play dual functions in the disease, whereby free radicals promote pathogen removal, but they can also trigger inflammation, resulting in tissue injuries. A growing body of evidence has strongly supported the notion that nuclear factor erythroid 2-related factor 2 (NRF) signaling is one of the main antioxidant pathways to combat this oxidative burst against parasites. Given the important role of NRF2 in oxidative stress, in this review, we investigate the activation mechanism of the NRF2 antioxidant pathway in different parasitic diseases, such as malaria, leishmaniasis, trypanosomiasis, toxoplasmosis, schistosomiasis, entamoebiasis, and trichinosis.
RESUMEN
Systemic lupus erythematosus (SLE) is a recognized chronic condition associated with immune system disorders that affect women nine times more commonly than men. SLE is characterized by over-secretion and release of autoantibodies in response to different cellular compartments and self-tolerance breaks to its own antigens. The detailed immunological dysregulation as an associated event that elicits the onset of clinical manifestations of SLE has not been clarified yet. Though, research using several animal models in the last two decades has indicated the role of the immune system in the pathogenesis of this disease. Myeloid-derived suppressor cells (MDSCs) as heterogeneous myeloid cells, are responsible for severe pathological conditions, including infection, autoimmunity, and cancer, by exerting considerable immunosuppressive effects on T-cells responses. It has been reported that these cells are involved in the regulation process of the immune response in several autoimmune diseases, particularly SLE. The function of MDSC is deleterious in infection and cancer diseases, though their role is more complicated in autoimmune diseases. In this review, we summarized the role and function of MDSCs in the pathogenesis and progression of SLE and its possible therapeutic approach.