Role of apoptosis in cardiac allograft vasculopathy

2000 ◽  
Vol 89 (0) ◽  
pp. IX21-IX23 ◽  
Author(s):  
D. Kabelitz
Keyword(s):  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy

Role of Genetics in Development of Cardiac Allograft Vasculopathy

2020 ◽  
Vol 39 (4) ◽  
pp. S76
Author(s):  
M. Pazdernik ◽  
J. Hubacek ◽  
P. Wohlfahrt ◽  
J. Kautzner ◽  
V. Melenovsky ◽  
...  
Keyword(s):  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy

scholarly journals Allograft or Recipient ST2 Deficiency Oppositely Affected Cardiac Allograft Vasculopathy via Differentially Altering Immune Cells Infiltration

2021 ◽  
Vol 12 ◽  
Author(s):  
Zhenggang Zhang ◽  
Na Zhang ◽  
Junyu Shi ◽  
Chan Dai ◽  
Suo Wu ◽  
...  
Keyword(s):  
T Cells ◽  
B Cells ◽  
Heart Transplantation ◽  
Immune Cells ◽  
Allograft Rejection ◽  
Vascular Occlusion ◽  
Cardiac Allograft Vasculopathy ◽  
Cardiac Allograft ◽  
Allograft Vasculopathy

The role of IL-33/ST2 signaling in cardiac allograft vasculopathy (CAV) is not fully addressed. Here, we investigated the role of IL-33/ST2 signaling in allograft or recipient in CAV respectively using MHC-mismatch murine chronic cardiac allograft rejection model. We found that recipients ST2 deficiency significantly exacerbated allograft vascular occlusion and fibrosis, accompanied by increased F4/80+ macrophages and CD3+ T cells infiltration in allografts. In contrast, allografts ST2 deficiency resulted in decreased infiltration of F4/80+ macrophages, CD3+ T cells and CD20+ B cells and thus alleviated vascular occlusion and fibrosis of allografts. These findings indicated that allografts or recipients ST2 deficiency oppositely affected cardiac allograft vasculopathy/fibrosis via differentially altering immune cells infiltration, which suggest that interrupting IL-33/ST2 signaling locally or systematically after heart transplantation leads different outcome.

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