The DOI matches its Crossref record; 65 of the 65 references it cites were found in a registry or an index.
Mechanisms of Rejection: Current Perspectives
Abstract
Rejection is the major barrier to successful transplantation. The immune response to an allograft is an ongoing dialogue between the innate and adaptive immune system that if left unchecked will lead to the rejection of transplanted cells, tissues, or organs. Activation of elements of the innate immune system, triggered as a consequence of tissue injury sustained during cell isolation or organ retrieval and ischemia reperfusion, will initiate and amplify the adaptive response. T cells require a minimum of two signals for activation, antigen recognition, and costimulation. The activation requirements of naive T cells are more stringent than those of memory T cells. Memory T cells are present in the majority of transplant recipients as a result of heterologous immunity. The majority of B cells require help from T cells to initiate antibody production. Antibodies reactive to donor human leukocyte antigen molecules, minor histocompatibility antigens, endothelial cells, RBCs, or autoantigens can trigger or contribute to rejection early and late after transplantation. Antibody-mediated rejection triggered by alloantibody binding and complement activation is recognized increasingly as a significant contribution to graft loss. Even though one component of the immune system may dominate and lead to rejection being described in short hand as T cell or antibody mediated, it is usually multifactorial resulting from the integration of multiple mechanisms. Identifying the molecular pathways that trigger tissue injury, signal transduction and rejection facilitates the identification of targets for the development of immunosuppressive drugs.
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“Nuclear and mitochondrial DNA, reactive oxygen species (ROS), and fragmented ECM components such as hyaluronic acid or fibronectin are among the most renowned DAMPs, which are released due to perturbation in the arrangement of nucleic acids within cells, transplantation imperfections such as ischemia-reperfusion, and harsh decellularization strategies, respectively [34–37].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [34]
In the citing paper
“The interaction of dECM scaffolds with the innate immune system is mainly mediated via damage-associated molecular patterns (DAMPs), danger signals released upon the cell and ECM damage during graft processing or implantation.”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [34]
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“However, innate immunity is insufficient for graft rejection and immunological traits of the implant, and its interplay with adaptive immunity will determine its fate [34, 39, 43].”
From Immunogenicity of decellularized extracellular matrix scaffolds: a bottleneck in tissue engineering and regenerative medicine (2023) · cites this paper as [34]
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Metadata
- Authors
- Wood, K. J., & Goto, R.
- Affiliations
- John Radcliffe Hospital (GB)
- Corresponding author
- Wood, Kathryn J.
- ORCID
- Goto, Ryoichi
- Venue
- Transplantation
- Published
- 2012-01-15
- Volume
- 93
- Issue
- 1
- Pages
- 1-10
- ISSN
- 0041-1337 (ISSN-L)
- OpenAlex
- W1973175840
- Cited by
- 369
- References
- 65
- Citations by year
- 2026: 12 · 2025: 14 · 2024: 18 · 2023: 19 · 2022: 14 · 2021: 22 · 2020: 25 · 2019: 24 · 2018: 27 · 2017: 27 · 2016: 25 · 2015: 36 · 2014: 43 · 2013: 32 · 2012: 31
- FWCI
- 6.11
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Transplantation (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Wellcome Trust
- British Heart Foundation
- Topics
- Health Sciences › Medicine › Surgery › Transplantation: Methods and Outcomes
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Transplantation › Renal Transplantation Outcomes and Treatments
- Keywords
- graft rejection, innate immune activation, adaptive immune response, T cell activation, costimulation, memory T cells, heterologous immunity, B cell help, antibody-mediated rejection, alloantibodies, complement activation, minor histocompatibility antigens, HLA antibodies, ischemia-reperfusion injury, graft loss
- MeSH terms
- B-Lymphocytes, Graft Rejection, Humans, Immunity, Innate, T-Lymphocytes, Signal Transduction, Organ Transplantation
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