Cytokine Overproduction, T-Cell Activation, and Defective T-Regulatory Functions Promote Nephritis in Systemic Lupus Erythematosus

Figure 1

Representation of pathogenetic mechanisms of lupus nephritis. LN is a disease that includes several mediators of glomerular inflammation. In this context, T-cell subsets, through the production of nephritogenic cytokines or by cooperating with B-cells, macrophages, and dendritic cells promote the activation of the glomerular immune response.