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Mohamed H. Sayegh

Researcher at Brigham and Women's Hospital

Publications -  488
Citations -  40228

Mohamed H. Sayegh is an academic researcher from Brigham and Women's Hospital. The author has contributed to research in topics: Transplantation & T cell. The author has an hindex of 103, co-authored 485 publications receiving 38540 citations. Previous affiliations of Mohamed H. Sayegh include Keele University & Alfaisal University.

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Endothelial-to-mesenchymal transition contributes to cardiac fibrosis

TL;DR: It is shown that cardiac fibrosis is associated with the emergence of fibroblasts originating from endothelial cells, suggesting an endothelial-mesenchymal transition (EndMT) similar to events that occur during formation of the atrioventricular cushion in the embryonic heart.
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Identification of cells initiating human melanomas

TL;DR: This work identifies a subpopulation enriched for human malignant-melanoma-initiating cells (MMIC) defined by expression of the chemoresistance mediator ABCB5 and shows that specific targeting of this tumorigenic minority population inhibits tumour growth.
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Tissue expression of PD-L1 mediates peripheral T cell tolerance

TL;DR: Evidence is provided that PD-L 1 expression on parenchymal cells rather than hematopoietic cells protects against autoimmune diabetes and point to a novel role for PD-1–PD-L1 interactions in mediating tissue tolerance.
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Oral Tolerance: Immunologic Mechanisms and Treatment of Animal and Human Organ-Specific Autoimmune Diseases by Oral Administration of Autoantigens

TL;DR: Orally administered autoantigens suppress several experimental autoimmune models in a disease- and antigen-specific fashion; the diseases include experimental autoimmune encephalomyelitis, uveitis, and myasthenia, collagen- and adjuvant-induced arthritis, and diabetes in the NOD mouse.
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Delayed graft function in kidney transplantation.

TL;DR: It is learnt that both ischaemia and reinstitution of blood flow in ischaemically damaged kidneys after hypothermic preservation activate a complex sequence of events that sustain renal injury and play a pivotal part in the development of delayed graft function.