Figure 1: Lymphocyte infiltration and antibody-mediated tissue damage contributes to the development of diabetic nephropathy (DN). The inflammatory environment generated by increased production of cytokines and chemokines in diabetes results in the recruitment of macrophages and T lymphocytes to the diabetic kidney (a) which further promotes the inflammatory process. Oxidation and glycosylation of native peptides ensues as a result of oxidative stress and hyperglycemia associated with the diabetes. These modified self peptides serve as novel antigens leading to production of B-cell derived autoantibodies that deposit in the glomerular basement membrane (GBM) (b) and generate circulating immune complexes (c). These autoantibodies may further promote inflammation and structural damage by activating complement and recruiting macrophages. Modified with permission from Cheung et al. [61].