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P8.073 (240.7 in Journal) Macrophages and different subtypes infiltrated in kidney allografts with antibody-mediated rejection

Puxun Tian, People's Republic of China

yuantian@mail.xjtu.edu.cn

Abstract

Macrophages and different subtypes infiltrated in kidney allografts with antibody-mediated rejection

Ge Deng1, Puxun Tian1, Meng Dou1, Bingxuan Zheng1, Huilin Gong2, Jin Zheng1.

1Department of Kidney Transplantation, Hospital of Nephropathy, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, People's Republic of China; 2Department of Pathology, The First Affiliated Hospital of Xi’an Jiaotong University, Xi’an, Shaanxi Province, People's Republic of China

Objective: To clarify the degree and location of total macrophages and subtypes infiltrated in the kidney allografts with antibody-mediated rejection (AMR) and its possible mechanisms.

Methods: There were three groups of renal biopsis, normal kidneys as the control group, renal allografts with stable renal function after kidney transplantation as the stable group and renal allografts with AMR diagnosed by biopsy after kidney transplantation as the AMR group. After fixed with 4% paraformaldehyde, embedded in paraffin and sectionalized, these tissues were stained using immunohistochemistry(IHC) to observe the positive degree and location of markers CD31 CD68 CD86 and CD206.

Results: Pathological changes in the three groups matched the previous description according to Hematoxylin-Eosin(HE) and Periodic Acid-Schiff stain (PAS) staining. Compared with the control group and stable group, the number of total macrophages (CD68+) infiltrated in the AMR group was significantly increased, and the infiltrated macrophages were mainly distributed around the microvessels (glomerulus and interstitial capillaries)(CD31+). Further classification of the infiltrated total macrophages in the AMR group showed that these macrophages were mainly pro-inflammatory M1 macrophages (CD68+CD86+), while the infiltration of tissue repair associated and anti-inflammatory M2 macrophages (CD68+CD206+) was not significant.

Conclusion: When AMR occurred in renal allografts, macrophages were mainly infiltrated around microvessels and they were largely pro-inflammatory M1 subtype. We hypothesized that chemotactic macrophages from endothelial cells of microvessels infiltrated into the transplanted kidney and were involved in the pathogenesis of AMR.

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