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Loss of regulatory T cell function on anti-inflammation is correlated with
increased risk of acute kidney injury development in patients with primary
glomerulonephritis
#MMPMID26221245
Dong Q
; Cai C
; Gao F
; Xu Z
; Fang Y
; Wang L
; Cui J
Int J Clin Exp Med
2015[]; 8
(5
): 7079-88
PMID26221245
show ga
Inflammation is believed to play a major role in the pathophysiology of acute
kidney injury (AKI). The injury induces the generation of inflammatory mediators
like cytokines and chemokines by tubular and endothelial cells which contribute
to the recruiting of leukocytes into the kidneys. Early AKI risk evaluation is
limited to demographic characteristics and past clinical histories, and no
specific treatment is available. To better identify patients at risk of
developing AKI, and devise more targeted treatment and prevention regimen, we
tracked 158 primary glomerulonephritis patients for their occurrence of AKI, and
analyzed the characteristics of their adaptive immune system. We found that in
patients that later developed AKI, peripheral blood T cell composition is shifted
toward IFN-g-producing Th1-like cells. While the composition of CD4(+)CD25(+) T
cells were similar between patients that later developed AKI and patients without
AKI development, in patients that later developed AKI, their CD4(+)CD25(+) T
cells secreted less regulatory cytokine IL-10, and was unable to suppress
proinflammatory cytokine production by CD4(+) T cells, while in patients without
AKI development, CD4(+)CD25(+) T cells were able to suppress CD4(+) T
cell-mediated IFN-g and IL-17 expression under stimulation, partially through
IL-10 secretion. Collectively, we identified a defect in CD4(+)CD25(+) T cell
regulatory function in patients at risk of developing AKI.
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