Pfeilschifter, J., Pignat, W., Vosbeck, K. and Marki, F. (1989) Interleukin 1 and Tumor Necrosis Factor Synergistically Stimulate Prostaglandin Synthesis and Phospholipase A2 Release from Rat Renal Mesangial Cells. Biochemical and Biophysical Research Communications, 159, 385-394.
http://dx.doi.org/10.1016/0006-291X(89)90003-X

has been cited by the following article:

• TITLE: Cytokines and T Helper Cells in Diabetic Nephropathy Pathogenesis

  AUTHORS: Liliane Silvano Araújo, Marcos Vinícius da Silva, Crislaine Aparecida da Silva, Maria Luiza Reis Monteiro, Lívia Helena de Morais Pereira, Laura Penna Rocha, Rosana Rosa Miranda Corrêa, Marlene Antônia Reis, Juliana Reis Machado

  KEYWORDS: Diabetic Nephropathy, Cytokines, Cellular Immunity

  JOURNAL NAME: Journal of Diabetes Mellitus, Vol.6 No.4, September 14, 2016

  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.