ABSTRACT
Diabetic
Nephropathy (DN) is considered the main cause of end stage kidney disease
around the world. However, its pathogenesis is not completely established. More
than just a direct consequence of chronic glycemic changes, recent studies had
suggested Diabetic Nephropathy could be considered an inflammatory disease. It
has been shown that concentrations of pro-inflammatory cytokines, as IL-1,
IL-6, IL-18, IL-33, IFN-γ and TNF-α actively participate in development and progression of DN, and thus, are
involved in pathogenesis. Besides, changes in acquired immune response,
especially the presence of cellular immune response profiles of pro-inflammatory
and effector nature, mainly Th1 and Th17, as the imbalance between interaction
of cytokines and T regulatory cells, foment the onset and progression of DN.
Here we summarize the main evidences that support the critical role of the
immune system in this condition. These new conceptual advances in DN
understanding are essential for development of new the rapeutical strategies
and prognostic factors, which could be protagonists or adjuvants to the current
ones, leading ultimately to a better clinical management of DN patients.
Share and Cite:
Araújo, L. , da Silva, M. , da Silva, C. , Monteiro, M. , de Morais Pereira, L. , Rocha, L. , Corrêa, R. , Reis, M. and Machado, J. (2016) Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis.
Journal of Diabetes Mellitus,
6, 230-246. doi:
10.4236/jdm.2016.64025.