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2018 ; 8
(1
): 5334
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CD4(+) and CD8(+) T Cells Exert Regulatory Properties During Experimental Acute
Aristolochic Acid Nephropathy
#MMPMID29593222
Baudoux T
; Husson C
; De Prez E
; Jadot I
; Antoine MH
; Nortier JL
; Hougardy JM
Sci Rep
2018[Mar]; 8
(1
): 5334
PMID29593222
show ga
Experimental aristolochic acid nephropathy is characterized by transient acute
proximal tubule necrosis and inflammatory cell infiltrates followed by
interstitial fibrosis and tubular atrophy. The respective role of T-cell
subpopulations has never been studied in the acute phase of the mouse model, and
was heretofore exclusively investigated by the use of several depletion
protocols. As compared to mice injected with aristolochic acids alone, more
severe acute kidney injury was observed after CD4(+) or CD8(+) T-cells depletion.
TNF-alpha and MCP-1 mRNA renal expressions were also increased. In contrast,
regulatory T-cells depletion did not modify the severity of the aristolochic
acids induced acute kidney injury, suggesting an independent mechanism.
Aristolochic acids nephropathy was also associated with an increased proportion
of myeloid CD11b(high)F4/80(mid) and a decreased proportion of their counterpart
CD11b(low)F4/80(high) population. After CD4(+) T-cell depletion the increase in
the CD11b(high)F4/80(mid) population was even higher whereas the decrease in the
CD11b(low)F4/80(high) population was more marked after CD8+ T cells depletion.
Our results suggest that CD4(+) and CD8(+) T-cells provide protection against
AA-induced acute tubular necrosis. Interestingly, T-cell depletion was associated
with an imbalance of the CD11b(high)F4/80(mid) and CD11b(low)F4/80(high)
populations.