Antibody-mediated Rejection
Antibody-mediated Rejection - Related Videos
08:42
A Standardized Murine Model with a Three-Person Workflow for Studying Acute Cellular and Antibody-Mediated Rejection in Xenotransplantation
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2026
This study establishes two standardized murine xenotransplantation models to specifically replicate acute cellular rejection and acute antibody-mediated rejection. These models serve as a reliable platform for investigating mechanisms of xenograft immune rejection, evaluating immunosuppressive strategies, and advancing preclinical xenotransplantation research.
05:21
Assessing Antibody-dependent, Cell-mediated Cytotoxicity in Cancer Cells using Antibody-Dependent Cell-Mediated Cytotoxicity Reporter Bioassay
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2024
Here, we present a protocol for an antibody-dependent, cell-mediated cytotoxicity (ADCC) assay using an ADCC bioassay kit. This method offers a valuable tool for elucidating the ADCC mechanism and evaluating the therapeutic potential of antibodies in cancer immunotherapy.
03:03
Measuring the Activation of Fc-Mediated Effector Functions by HA Antibodies
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2025
This video demonstrates an assay measuring the antibody-mediated activation of T cell effector functions. Adding an influenza virus hemagglutinin (HA)-specific monoclonal antibody to transfected mammalian cells expressing HA results in the formation of immune complexes with HA. Upon introducing engineered T cells expressing Fc receptors and a luciferase reporter, the T cells are activated by the antibody-HA complexes, and this activation is detected by adding a luciferase substrate and...
07:18
Cell-based Assay to Study Antibody-mediated Tau Clearance by Microglia
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Cited by 6 •
2018
Here we describe a cell-based assay to quantitatively assess tau uptake by microglia with the aim of creating an investigational tool to better characterize the mechanisms of action of anti-tau antibodies.
07:05
Mouse Model of Alloimmune-induced Vascular Rejection and Transplant Arteriosclerosis
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Cited by 7 •
2015
We describe a protocol for aortic interposition grafting in mice. The goal of the protocol is to provide a model with which to study pathological processes and therapeutic strategies relevant to alloimmune reactions in arteries and the resultant arterial changes that contribute to organ transplant failure.
FAQs
Complement activation links antibody binding to vascular injury in the graft. After donor-specific antibodies recognize antigens on endothelial cells, complement and other immune effector cells contribute to microvascular inflammation. This process can impair blood flow, damage tissue, and, in some cases, promote thrombosis, helping explain why graft performance may decline.
Endothelial cells line the graft’s blood vessels and are directly exposed to donor-specific antibodies. Their involvement places the initial immune attack within the graft microvasculature, rather than limiting injury to a single tissue compartment. Resulting vascular inflammation provides a mechanistic link between antibody recognition, tissue damage, and threatened graft survival.
Microvascular inflammation and tissue injury can reduce the graft’s ability to function normally, while thrombosis can further compromise its blood supply. Because these changes threaten graft survival, clinicians treat altered graft performance as an important signal to investigate alongside antibody results and biopsy findings rather than relying on a single indicator.
Clinicians interpret suspected antibody-mediated rejection by combining biopsy findings, antibody tests, and changes in graft performance. Biopsy information can reveal tissue injury, antibody testing can identify relevant donor-specific antibodies, and functional changes show whether the graft is being affected. Considering these findings together supports more informed transplant monitoring.
Treatment strategies can target either the antibodies or the broader immune response. Antibody removal may reduce the factors attacking the graft, while immunosuppression can help limit immune activity. Controlling these processes may protect graft function and survival, making treatment selection an important part of ongoing transplant management.
Reducing antibody formation is important because fewer donor-specific antibodies may lessen the opportunity for endothelial binding and downstream vascular injury. This preventive focus complements treatment after injury has appeared. In research, the same principle supports investigation of immune tolerance, an approach intended to improve transplant outcomes by limiting harmful responses to the graft.