Role of Complement Activation in Allograft Inflammation

Nicholas H. Chun, Julian K. Horwitz, Peter S. Heeger

Research output: Contribution to journalReview articlepeer-review

3 Scopus citations


Purpose of Review: Novel paradigms have broadened our understanding of mechanisms through which complement mediates allograft inflammation/injury. Herein, we review advances in the field and highlight therapeutic implications. Recent Findings: Pre-clinical and translational human trials have elucidated complement-dependent mechanisms of post-transplant ischemia-reperfusion (I/R) injury. Immune cell-derived, and intracellular, complement activation is newly linked to proinflammatory T cell immunity relevant to allograft rejection. Complement-induced immune regulation, including C5a ligation of C5a receptor 2 on T cells, C5a/C5a receptor 1 interactions on regulatory myeloid cells, and C1q binding to CD8+ T cells, can inhibit proinflammatory T cells and/or prolong murine allograft survival. Pilot trials of complement inhibition to treat/prevent human I/R- or antibody-initiated allograft injury show promise. Summary: The complement system participates in allograft injury through multiple context-dependent mechanisms involving various components and receptors. These new insights along with development and implementation of individualized complement inhibitory strategies have potential to improve transplant outcomes.

Original languageEnglish
Pages (from-to)52-59
Number of pages8
JournalCurrent Transplantation Reports
Issue number1
StatePublished - 15 Mar 2019


  • Allograft inflammation
  • Antibody-mediated rejection
  • Complement
  • Ischemia reperfusion injury
  • T cell activation


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