Intragraft immune cells: accomplices or antagonists of recipient-derived macrophages in allograft fibrosis?

Abstract

Organ fibrosis caused by chronic allograft rejection is a major concern in the field of transplantation. Macrophage-to-myofibroblast transition plays a critical role in chronic allograft fibrosis. Adaptive immune cells (such as B and CD4+ T cells) and innate immune cells (such as neutrophils and innate lymphoid cells) participate in the occurrence of recipient-derived macrophages transformed to myofibroblasts by secreting cytokines, which eventually leads to fibrosis of the transplanted organ. This review provides an update on the latest progress in understanding the plasticity of recipient-derived macrophages in chronic allograft rejection. We discuss here the immune mechanisms of allograft fibrosis and review the reaction of immune cells in allograft. The interactions between immune cells and the process of myofibroblast formulation are being considered for the potential therapeutic targets of chronic allograft fibrosis. Therefore, research on this topic seems to provide novel clues for developing strategies for preventing and treating allograft fibrosis.

Reduction in myocardial fibrosis in MDX mice on oral consumption ofAureobasidium Pullulansproduced Neu REFIX Beta-glucans; holds potential as an adjuvant in managing post-transplantation organ fibrosis

“…Hypoxia, in turn, has been shown to induce phenotypic changes consistent with endothelial-tomesenchymal transition (EndMT), in which ECs undergo phenotypic changes and transdifferentiate into myofibroblast-like cells with increased extracellular matrix protein production, contributing to fibrosis [12]. Also, by secreting cytokines, adaptive immune cells (such as B and CD4+ T cells) and innate immunity cells (such as neutrophils and innate lymphoid cells) contribute to the trans differentiation of 10 recipient-derived macrophages to myofibroblasts, which leads to transplanted organ fibrosis [13].…”

“…CC-BY-NC-ND 4.0 International license perpetuity. It is made available under a preprint (which was not certified by peer review) is the author/funder, who has granted bioRxiv a license to display the preprint in The copyright holder for this this version posted September 28, 2023. ; https://doi.org/10.1101/2023.09.25.559276 doi: bioRxiv preprint 10 recipient-derived macrophages to myofibroblasts, which leads to transplanted organ fibrosis [13].…”

“…Hypoxia, in turn, has been shown to induce phenotypic changes consistent with endothelial-to-mesenchymal transition (EndMT), in which ECs undergo phenotypic changes and transdifferentiate into myofibroblast-like cells with increased extracellular matrix protein production, contributing to fibrosis [12]. Also, by secreting cytokines, adaptive immune cells (such as B and CD4+ T cells) and innate immunity cells (such as neutrophils and innate lymphoid cells) contribute to the trans differentiation of recipient-derived macrophages to myofibroblasts, which leads to transplanted organ fibrosis [13]. Although the mechanisms leading to chronic allograft rejection including the role of innate immune mechanisms including macrophage and NK cell activation and antibody mediated rejection are better understood, there has been little progress in the treatment of chronic allograft rejection.…”

The role and research progress of macrophages after heart transplantation

“…Additionally, the activation of the colony-stimulating factor receptor-1 (CSF-1R) signaling axis is essential for the differentiation of Ly6Chigh monocytes into Ly6Clow CX3CR1 high monocytes. These signaling pathways play a central role in the proliferation and chemotaxis of M2-like macrophages upon stimulation [ 61 , 62 ].…”