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CD4 + and CD8 + T Cells Exert Regulatory Properties During Experimental Acute Aristolochic Acid Nephropathy
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,...
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Published in: | Scientific reports 2018-03, Vol.8 (1), p.5334-12, Article 5334 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | 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
F4/80
and a decreased proportion of their counterpart CD11b
F4/80
population. After CD4
T-cell depletion the increase in the CD11b
F4/80
population was even higher whereas the decrease in the CD11b
F4/80
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
F4/80
and CD11b
F4/80
populations. |
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ISSN: | 2045-2322 2045-2322 |
DOI: | 10.1038/s41598-018-23565-2 |