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^highF4/80^mid and a decreased proportion of their counterpart CD11b^lowF4/80^high population. After CD4⁺ T-cell depletion the increase in the CD11b^highF4/80^mid population was even higher whereas the decrease in the CD11b^lowF4/80^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^highF4/80^mid and CD11b^lowF4/80^high populations.