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Barbara A. Wasowska

Researcher at Johns Hopkins University

Publications -  44
Citations -  2229

Barbara A. Wasowska is an academic researcher from Johns Hopkins University. The author has contributed to research in topics: Transplantation & Complement system. The author has an hindex of 22, co-authored 40 publications receiving 2161 citations. Previous affiliations of Barbara A. Wasowska include Beth Israel Deaconess Medical Center & Duke University.

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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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Cytokines, adhesion molecules, and the pathogenesis of chronic rejection of rat renal allografts.

TL;DR: It is concluded that cytokine production and upregulation of adhesion molecules occurring as part of a cellular immune response may be as important, to the etiology of chronic rejection as the hitherto widely emphasized antibody-mediated host responses.
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Antibody to human leukocyte antigen triggers endothelial exocytosis

TL;DR: The data show that antibody to host antigens can activate human endothelial cell exocytosis and leukocyte trafficking, and by triggering vascular inflammation, antibody activation of exocyTosis may play a role in transplant rejection.
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Passive transfer of alloantibodies restores acute cardiac rejection in IgKO mice.

TL;DR: A model of alloantibody-mediated graft injury is established using B10.A hearts transplanted to wild type or immunoglobulin knock out (IgKO) mice, indicating that macrophage- and T-cell-dependent immune responses were intact in IgKO recipients.
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Non-complement- and complement-activating antibodies synergize to cause rejection of cardiac allografts.

TL;DR: 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.