Complement factor and T-cell interactions during alloimmune inflammation in transplantation

J Leukoc Biol. 2019 Apr;105(4):681-694. doi: 10.1002/JLB.5RU0718-288R. Epub 2018 Dec 11.

Abstract

Complement factor and T-cell signaling during an effective alloimmune response plays a key role in transplant-associated injury, which leads to the progression of chronic rejection (CR). During an alloimmune response, activated complement factors (C3a and C5a) bind to their corresponding receptors (C3aR and C5aR) on a number of lymphocytes, including T-regulatory cells (Tregs), and these cell-molecular interactions have been vital to modulate an effective immune response to/from Th1-effector cell and Treg activities, which result in massive inflammation, microvascular impairments, and fibrotic remodeling. Involvement of the complement-mediated cell signaling during transplantation signifies a crucial role of complement components as a key therapeutic switch to regulate ongoing inflammatory state, and further to avoid the progression of CR of the transplanted organ. This review highlights the role of complement-T cell interactions, and how these interactions shunt the effector immune response during alloimmune inflammation in transplantation, which could be a novel therapeutic tool to protect a transplanted organ and avoid progression of CR.

Keywords: T-cell activation; complement mediators; costimulatory signals.

Publication types

  • Review

MeSH terms

  • Animals
  • Cell Communication*
  • Complement System Proteins / metabolism*
  • Humans
  • Inflammation / immunology*
  • Inflammation / pathology*
  • Lymphocyte Activation / immunology
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology
  • Transplantation*

Substances

  • Complement System Proteins