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T cell infiltration is associated with kidney injury in patients with anti-glomerular basement membrane disease

Abstract

Cell-mediated autoimmunity, particularly that involving autoreactive T cells, participates in mediating anti-glomerular basement membrane (GBM) disease. However, direct kidney injury mediated by renal infiltrated T cells has not been clearly elucidated in humans. The T cell profile (CD3, CD4, CD8, IL-17, and foxp3) and macrophage (CD68) were examined by immunohistochemistry on renal biopsy tissues from 13 patients with anti-GBM disease. The correlation between cell infiltration and clinical data was also analyzed. We found that the distribution of T cell infiltration was predominant in the peri-glomerular and interstitial areas. CD3+ T cell infiltratrion around the glomeruli with cellular crescent formations was significantly higher than that around the glomeruli with mild mesangial proliferation. CD8+ T cells significantly accumulated around the glomeruli with cellular crescents without IgG deposits compared to those with IgG deposits. The prevalence of infiltrating CD8+ T cells was correlated with the percentage of ruptured Bowman’s capsules. In conclusion, cellular immunity may play a crucial role in the inflammatory kidney injury in anti-GBM patients. The periglomerular infiltration of T cells, especially CD8+ T cells, may participate in the pathogenic mechanism of glomerular damage.

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Acknowledgements

The authors greatly appreciate the technical support provided by Miao Wang from Renal Division, Department of Medicine, Peking University First Hospital. This work was supported by the National Basic Research Program of China (2012CB517702), the Natural Science Foundation of China (81321064,81330020, 81370801, 81400703).

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Correspondence to Zhao Cui.

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Hu, SY., Jia, XY., Li, JN. et al. T cell infiltration is associated with kidney injury in patients with anti-glomerular basement membrane disease. Sci. China Life Sci. 59, 1282–1289 (2016). https://doi.org/10.1007/s11427-016-5030-9

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  • DOI: https://doi.org/10.1007/s11427-016-5030-9

Keywords

  • anti-GBM disease
  • T cell
  • IL-17
  • CD8
  • kidney injury