ZBTB20 regulates cardiac allograft rejection through NFкB-mediated inflammation in mouse heart transplantation
Liuyi Lu, Maomao Shi, Junxiong Qiu, Zhanyue Shi, Chao Wang, Yuan Fu, Canxiang Lin, Lisui Zhang, Jun Tao, Chang Liu, Feng Wei, Shi Liang, Junmeng Zheng
Journal:TRANSPLANT IMMUNOLOGY
IF:2.03
DOI:10.1016/j.trim.2022.101676
PMID:35872083
Published:2022-07-22
research field:分子生物学转化医学细胞治疗心血管病学免疫学再生医学
Abstract
Allograft rejection is a major obstacle for the long-term survival of heart transplantation (Htx) patients . The cardiac allograft rejection requires the activation of macrophages and effector T cells . In this study, we explored the role of zinc-finger and BTB domain containing protein 20 (ZBTB20) in the regulation of heart allograft rejection. Flow cytometry analysis of the spleen cells from mice undergoing an acute cardiac rejection revealed that the ZBTB20 protein expression was upregulated in both T and B cells( n = 4, P < 0.01). In addition, ZBTB20 gene knockdown significantly prolonged the survival of heart allografts in mice( n = 4, P < 0.01). Lack of ZBTB20 increased the expression of Foxp3 and limited the response of T helper 1 (Th1) cells(n = 4, P < 0.01). The ZBTB20-related regulation occurred through the activation of the NFкB pathway. In conclusion, our data suggest that ZBTB20 is involved in the regulation of T cells involved in acute heart allograft rejection. Hence, downregulation of ZBTB20 expression may inhibit T cells to prolong heart transplant survival .
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