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2017 ; 7
(1
): 11683
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Changes in CD73, CD39 and CD26 expression on T-lymphocytes of ANCA-associated
vasculitis patients suggest impairment in adenosine generation and turn-over
#MMPMID28916770
Kling L
; Benck U
; Breedijk A
; Leikeim L
; Heitzmann M
; Porubsky S
; Krämer BK
; Yard BA
; Kälsch AI
Sci Rep
2017[Sep]; 7
(1
): 11683
PMID28916770
show ga
Extracellular adenosine, generated via the concerted action of CD39 and CD73,
contributes to T-cell differentiation and function. Adenosine concentrations are
furthermore influenced by adenosine deaminase binding protein CD26. Because
aberrant T-cell phenotypes had been reported in anti-neutrophil cytoplasmic
auto-antibody (ANCA)-associated vasculitis (AAV) patients, an impaired expression
of these molecules on T-cells of AAV patients was hypothesized in the present
study. While in AAV patients (n?=?29) CD26 was increased on CD4(+) lymphocytes,
CD39 and CD73 were generally reduced on patients' T-cells. In CD4(+) cells
significant differences in CD73 expression were confined to memory CD45RA(-)
cells, while in CD4(-) lymphocytes differences were significant in both naïve
CD45RA(+) and memory CD45RA(-) cells. The percentage of CD4(-)CD73(+) cells
correlated with micro-RNA (miR)-31 expression, a putative regulator of factor
inhibiting hypoxia-inducible factor 1 alpha (FIH-1), inversely with serum
C-reactive protein (CRP) and positively with estimated glomerular filtration rate
(eGFR). No correlation with disease activity, duration, and ANCA profile was
found. It remains to be assessed if a decreased CD73 and CD39 expression
underlies functional impairment of lymphocytes in AAV patients. Likewise, the
relations between frequencies of CD4(-)CD73(+) cells and serum CRP or eGFR
require further functional elucidation.