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

SY Hu, XY Jia, JN Li, X Zheng, J Ao, G Liu… - Science China Life …, 2016 - Springer
SY Hu, XY Jia, JN Li, X Zheng, J Ao, G Liu, Z Cui, MH Zhao
Science China Life Sciences, 2016Springer
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 …
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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