PubMed Health⌕ Search
Home/Archive/PubMed

PubMed · 8019031

Chronic allograft rejection: an update.

P Häyry
View original source ↗Export metadata ↓

Abstract

The etiology of chronic rejection is most probably multifactorial. The common feature in all organ allografts undergoing chronic rejection is persistent perivascular inflammation and a concentric generalized arteriosclerosis affecting all first and second order intramural arteries. A hypothesis is presented that low-grade damage to endothelium induces the secretion of growth factors which, in turn, are responsible for smooth muscle cell replication and their influx into intima.

Explore related subjects

Graft RejectionHumansTransplantation, HomologousJournal ArticleReview

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P Häyry. 1994. Chronic allograft rejection: an update.. https://pubmed.ncbi.nlm.nih.gov/8019031/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

PubMed2026

Hypoimmune platforms: from rejection to immune evasion and regulatory implications.

The growing gap between organ demand and clinical availability has renewed interest in immune-evasive graft strategies, yet rejection and lifelong immunosuppression remain major barriers to durable success. Advances in genome editing enable immune-evasive cell platforms designed to avoid immune recognition while replacing missing function in allogeneic settings. This review summarizes current strategies for engineering immune-evasive grafts that simultaneously suppress adaptive and innate immune responses. We discuss how coordinated modulation of antigen presentation and immune checkpoint pathways can protect transplanted allogeneic cells and tissues from T, NK, and macrophage-mediated rejection. We also present the emerging concept of integrating hypoimmune engineering with genetically modified porcine donors, where extensive genome editing has reduced, but not eliminated, xenogeneic immune barriers. Combining donor genome modification with immune-evasive graft design represents a promising conceptual advance toward xenograft survival, though whether full elimination of systemic immunosuppression is achievable remains to be established clinically. We further examine how the regulatory landscape for these products is evolving across major jurisdictions, and how differences in approval pathways, manufacturing standards, and long-term surveillance requirements shape the path to clinical translation. Finally, we outline the safety considerations and remaining limitations in immune evasion that must be addressed to enable clinical implementation.

Graft Rejection↗
PubMed2007

The classification and treatment of antibody-mediated renal allograft injury: where do we stand?

Since the acceptance of the detection of C4d in allografts as a reliable tool to mark a humoral alloresponse, de novo antibody-induced graft injury has attracted much attention. Antibodies and B cells are the new frontier in transplantation. At this juncture carefully designed studies are critical in order to gain solid diagnostic, therapeutic, and prognostic knowledge about the role of antibodies in graft injury and to avoid any confusion and misconception. One prerequisite is the strict adherence to refined classification systems of renal transplant rejection that carefully split and categorize different phenotypes of humoral mediated graft damage and ideally also include information on anti-donor antibody specificity and titers. Sun and colleagues follow this concept and provide evidence that mixed cellular and antibody-mediated graft rejection can respond favorably to intensified immunosuppression with tacrolimus and mycophenolate mofetil. What will the future bring to treat rejection episodes with a dominant, co-dominant, or minor antibody response?

Graft Rejection↗