Vitamin D and immune function in chronic kidney disease

Wen Chih Liu, Cai Mei Zheng, Chien Lin Lu, Yuh Feng Lin, Jia Fwu Shyu, Chia Chao Wu, Kuo Cheng Lu

研究成果: 雜誌貢獻回顧型文獻同行評審

24 引文 斯高帕斯(Scopus)


The common causes of death in chronic kidney disease (CKD) patients are cardiovascular events and infectious disease. These patients are also predisposed to the development of vitamin D deficiency, which leads to an increased risk of immune dysfunction. Many extra-renal cells possess the capability to produce local active 1,25(OH)2D in an intracrine or paracrine fashion, even without kidney function. Vitamin D affects both the innate and adaptive immune systems. In innate immunity, vitamin D promotes production of cathelicidin and β-defensin 2 and enhances the capacity for autophagy via toll-like receptor activation as well as affects complement concentrations. In adaptive immunity, vitamin D suppresses the maturation of dendritic cells and weakens antigen presentation. Vitamin D also increases T helper (Th) 2 cytokine production and the efficiency of Treg lymphocytes but suppresses the secretion of Th1 and Th17 cytokines. In addition, vitamin D can decrease autoimmune disease activity. Vitamin D has been shown to play an important role in maintaining normal immune function and crosstalk between the innate and adaptive immune systems. Vitamin D deficiency may also contribute to deterioration of immune function and infectious disorders in CKD patients. However, it needs more evidence to support the requirements for vitamin D supplementation.
頁(從 - 到)135-144
期刊Clinica Chimica Acta
出版狀態已發佈 - 10月 23 2015

ASJC Scopus subject areas

  • 生物化學
  • 臨床生物化學
  • 生物化學(醫學)


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