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Open AccessJournal ArticleDOI

Non-complement- and complement-activating antibodies synergize to cause rejection of cardiac allografts.

TLDR
Non‐complement‐activating AlloAbs stimulate endothelial cells to produce chemokines and this effect is augmented in the milieu of proinflammatory cytokines, indicating that non-complement •activating •AlloAbs can augment injury to allografts by complement‐activated Allo Abs.
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This article is published in American Journal of Transplantation.The article was published on 2004-03-01 and is currently open access. It has received 92 citations till now. The article focuses on the topics: Complement system & Proinflammatory cytokine.

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Banff '09 meeting report: Antibody mediated graft deterioration and implementation of Banff working groups

TL;DR: The willingness of the Banff process to adapt continuously in response to new research and improve potential weaknesses, led to the implementation of six working groups on the following areas: isolated v‐lesion, fibrosis scoring, glomerular lesions, molecular pathology, polyomavirus nephropathy and quality assurance.
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Antibody-Mediated Renal Allograft Rejection: Diagnosis and Pathogenesis

TL;DR: Substantial practical experience by pathologists in the interpretation and pitfalls of C4d stains are reviewed along with considerations of the clinical significance and pathologic mechanisms of the different effects of antibody on the endothelium of the renal allograft.
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Antibody-mediated organ-allograft rejection

TL;DR: Antibody induces rejection acutely through the fixation of complement, resulting in tissue injury and coagulation, and complement activation recruits macrophages and neutrophils, causing additional endothelial injury.
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De novo donor HLA-specific antibodies after heart transplantation are an independent predictor of poor patient survival.

TL;DR: Patients who are transplanted in the absence of pre‐existing DSA make de novo DSA after transplantation which are associated with poor survival, and early and regular monitoring of post‐transplant DSA is required to identify patients at risk of allograft failure.
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IgG Donor-Specific Anti-Human HLA Antibody Subclasses and Kidney Allograft Antibody-Mediated Injury

TL;DR: IgG iDSA subclasses identify distinct phenotypes of kidney allograft antibody-mediated injury as well as HLA class specificity, MFI level, C1q-binding status, and IgG subclasses in a Cox survival model are revealed.
References
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Journal ArticleDOI

A B cell-deficient mouse by targeted disruption of the membrane exon of the immunoglobulin μ chain gene

TL;DR: The importance of the membrane form of the μ chain in B-cell development is assessed by generating mice lacking this chain by disrupting one of the membranes exons of the gene encoding the μ-chain constant region by gene targeting in mouse embryonic stem cells.
Journal Article

Hybridoma cell lines secreting monoclonal antibodies to mouse H-2 and Ia antigens.

TL;DR: Strain distribution analyses so far indicate that the public specificities detected by these monoclonal antibodies are considerably different from those that had been established by traditional serology, which may have important implications relating to the structure and evolution of MHC gene products.
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Human IgG Fc receptor heterogeneity: molecular aspects and clinical implications.

TL;DR: Receptors for the Fc domain of IgG (Fc gamma R) provide a critical link between specific humoral responses and the cellular branch of the immune system and, importantly, recent evidence points at the relevance of this Fc Gamma R heterogeneity.
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Plasmapheresis and intravenous immune globulin provides effective rescue therapy for refractory humoral rejection and allows kidneys to be successfully transplanted into cross-match-positive recipients

TL;DR: This protocol shows promise for eliminating DSA preemptively among patients with low-titer positive antihuman globulin-enhanced, complement-dependent cytotoxicity cross-matches, allowing the successful transplantation of these patients using a live donor without any cases of HAR.
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