Orthotopic heart transplant rejection in association with immunomodulatory therapy for AL amyloidosis: A case series and review of the literature

2019 ◽  
Vol 19 (11) ◽  
pp. 3185-3190 ◽  
Author(s):  
David A. Qualls ◽  
Gregory D. Lewis ◽  
Vaishali Sanchorawala ◽  
Andrew Staron
Author(s):  
Kevin J. Clerkin ◽  
Maryjane A. Farr

This chapter focuses on orthotopic heart transplant rejection. Hyperacute rejection is a catastrophic complication that occurs early post-transplantation. This type of rejection is most often due to pre-formed donor-specific anti–human leukocyte antigen antibodies or an ABO blood type mismatch and is rarely seen in the current era because pre-transplant virtual and prospective crossmatch has become routine practice. Meanwhile, immune activation of recipient T cells against the cardiac allograft causes acute cellular rejection (ACR). Treatment of ACR will vary depending on the grade of rejection, symptoms, and hemodynamic significance. On the other hand, antibody-mediated rejection (AMR), previously known as humoral or vascular rejection, is primarily mediated by antibodies and not T cells, as in ACR. AMR is difficult to treat because it may persist or be recurrent and is associated with an increased risk of cardiac allograft vasculopathy and mortality. The chapter then discusses the management of acute rejection. Induction therapy is augmented immunosuppression in the early period following heart transplantation, when the recipient is at the greatest risk of rejection. Maintenance immunosuppression includes calcineurin inhibitors, anti-metabolites, glucocorticoids, and proliferation signal inhibitors.


2005 ◽  
Vol 24 (2) ◽  
pp. 160-165 ◽  
Author(s):  
Jing Ping Sun ◽  
Ibrahim A. Abdalla ◽  
Craig R. Asher ◽  
Neil L. Greenberg ◽  
Zoran B. Popović ◽  
...  

2021 ◽  
Vol 7 (1) ◽  
Author(s):  
Jian Lu ◽  
Weiwei Wang ◽  
Peiyuan Li ◽  
Xiaodong Wang ◽  
Chao Gao ◽  
...  

AbstractRegulatory T cells (Tregs), which characteristically express forkhead box protein 3 (Foxp3), are essential for the induction of immune tolerance. Here, we investigated microRNA-146a (miR-146a), a miRNA that is widely expressed in Tregs and closely related to their homeostasis and function, with the aim of enhancing the function of Tregs by regulating miR-146a and then suppressing transplant rejection. The effect of the absence of miR-146a on Treg function in the presence or absence of rapamycin was detected in both a mouse heart transplantation model and cell co-cultures in vitro. The absence of miR-146a exerted a mild tissue-protective effect by transiently prolonging allograft survival and reducing the infiltration of CD4+ and CD8+ T cells into the allografts. Meanwhile, the absence of miR-146a increased Treg expansion but impaired the ability of Tregs to restrict T helper cell type 1 (Th1) responses. A miR-146a deficiency combined with interferon (IFN)-γ blockade repaired the impaired Treg function, further prolonged allograft survival, and alleviated rejection. Importantly, miR-146a regulated Tregs mainly through the IFN-γ/signal transducer and activator of transcription (STAT) 1 pathway, which is implicated in Treg function to inhibit Th1 responses. Our data suggest miR-146a controls a specific aspect of Treg function, and modulation of miR-146a may enhance Treg efficacy in alleviating heart transplant rejection in mice.


1994 ◽  
Vol 40 ◽  
pp. 8
Author(s):  
S. Sheldon ◽  
P. Haselton ◽  
N.A. Yonan ◽  
A.N. Rahman ◽  
A.K. Deiraniya ◽  
...  

Gene Therapy ◽  
2001 ◽  
Vol 8 (22) ◽  
pp. 1738-1744 ◽  
Author(s):  
JL Bracy ◽  
CM Chase ◽  
PS Russell ◽  
S Mauiyyedi ◽  
RB Colvin ◽  
...  

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