Journal
AMERICAN JOURNAL OF TRANSPLANTATION
Volume 22, Issue -, Pages 12-17Publisher
WILEY
DOI: 10.1111/ajt.17206
Keywords
basic (laboratory) research; science; cytokines; cytokine receptors; heart (allograft) function; dysfunction; heart transplantation; cardiology; immunosuppression; immune modulation; immunosuppressant-fusion proteins and monoclonal antibodies; rejection; acute; chronic; solid organ transplantation; translational research
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Funding
- Translational Fellowship Research Grant
- National Heart, Lung, and Blood Institute [P01 HL158504]
- National Institute of Allergy and Infectious Diseases [P01 AI123086, R25 AI147393, U01 AI131470]
- Thoracic Surgery Foundation
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Outcomes of heart transplantation remain suboptimal due to acute and chronic rejection. IL-6, a pro-inflammatory cytokine, plays a critical role in allograft injury and immune response after heart transplantation. Inhibiting IL-6 signaling has emerged as a promising strategy to prevent rejection and improve outcomes in heart transplant recipients.
Outcomes following heart transplantation remain suboptimal with acute and chronic rejection being major contributors to poor long-term survival. IL-6 is increasingly recognized as a critical pro-inflammatory cytokine involved in allograft injury and has been shown to play a key role in regulating the inflammatory and alloimmune responses following heart transplantation. Therapies that inhibit IL-6 signaling have emerged as promising strategies to prevent allograft rejection. Here, we review experimental and pre-clinical evidence that supports the potential use of IL-6 signaling blockade to improve outcomes in heart transplant recipients.
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