|Support type:||Scholarships in Brazil - Doctorate|
|Effective date (Start):||December 01, 2012|
|Effective date (End):||June 30, 2015|
|Field of knowledge:||Health Sciences - Medicine|
|Principal researcher:||Maria Aparecida Dalboni|
|Grantee:||José Tarcísio Giffoni de Carvalho Júnior|
|Home Institution:||Escola Paulista de Medicina (EPM). Universidade Federal de São Paulo (UNIFESP). Campus São Paulo. São Paulo , SP, Brazil|
Cardiovascular (CV) and infectious diseases remain the most common causes of mortality and morbidity, respectively among patients with chronic kidney disease (CKD). Previous studies have reported several alterations in immune cells, which contribute to increase incidence of CV and infectious diseases observed in this population. Biocompatibility of dialysis membrane and uremic toxins are the main factors associated with immune dysfunction in uremia. Furthermore, the Vitamin D deficiency is also associated with immunologic co-morbidities that are present in CKD. Vitamin D deficiency is highly prevalent among patients with all stages of CKD, but it is greater in peritoneal dialysis (PD) patients than the hemodialysis (HD) and pre-dialysis CKD patients. As the vitamin D receptor is expressed in the immune cells (B cells, T cells and others), and these cells are able to synthesizing the active vitamin D metabolite, many studies have investigated the role of vitamin D in the immune system. In this regard, previous studies have reported that vitamin D inhibits the TLR-induced cytokines production, including IFN-³ and IL-6. Thus, the purpose or this study is evaluate the effect of cholecalciferol treatment therapy on apoptosis, IFN-³ and IL-6 production, TLR-7 and TLR-9 expression in lymphocytes B in vitro and in vivo.