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Journal of Immunology Research
Volume 2014, Article ID 582902, 10 pages
Research Article

Capillary Dilation and Rarefaction Are Correlated with Intracapillary Inflammation in Antibody-Mediated Rejection

1National Clinical Research Center of Kidney Diseases, Jinling Hospital, Nanjing University Clinical School of Medicine, 305 East Zhong Shan Road, Nanjing 210002, China
2Department of Renal Transplantation, The Third Affiliated Hospital, Sun Yat-Sen University, Guangzhou 510760, China

Received 22 June 2013; Accepted 31 December 2013; Published 10 February 2014

Academic Editor: Xian Li

Copyright © 2014 Xue Li et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Antibody-mediated rejection (ABMR) remains one of the major causes of graft loss after renal transplantation. It is dominated by endothelial damage in microcirculation. Clarifying the mechanism of microcirculating damage is obviously a key step to understand the pathogenesis of ABMR. Here we characterized capillary variation in ABMR and its possible mechanisms. Compared with T cell-mediated rejection and stable grafts, there was a significant dilation and rarefaction in peritubular capillaries (PTCs) of the ABMR group; Image-Pro Plus revealed a significantly larger intra-PTC area. Interestingly, the dilation of PTCs was strongly correlated with the intra-PTC cell counting. Moreover, peritubular capillary inflammation is correlated with in situ T-bet expression, and there was a good correlation between the intra-PTC expression of T-bet and the PTC diameter. HIF-1α up-regulation could be observed in ABMR but it was not necessary for capillary dilation. In general, ABMR is characterized with early capillary dilation and rarefaction; our data confirmed that the dilation is strongly correlated with intracapillary inflammation, which in turn is correlated with in situ T-bet expression. T-bet plays an important role in the development of microcirculating injury, and thus it is a potential target for the treatment of ABMR.