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Sussan Nourshargh

Researcher at Queen Mary University of London

Publications -  148
Citations -  16130

Sussan Nourshargh is an academic researcher from Queen Mary University of London. The author has contributed to research in topics: Inflammation & Cell adhesion molecule. The author has an hindex of 59, co-authored 146 publications receiving 14197 citations. Previous affiliations of Sussan Nourshargh include National Institutes of Health & University of Cambridge.

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Platelet-endothelial cell adhesion molecule-1 (PECAM-1)-deficient mice demonstrate a transient and cytokine-specific role for PECAM-1 in leukocyte migration through the perivascular basement membrane.

TL;DR: A regulatory role for PECAM-1 is suggested in leukocyte migration through the perivascular basement membrane, a role that appears to be cytokine-specific and associated with the ability of the cytokine to stimulate rapid neutrophil adhesion.
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Leukotriene B4-Neutrophil Elastase Axis Drives Neutrophil Reverse Transendothelial Cell Migration In Vivo

TL;DR: It is demonstrated that the lipid chemoattractant leukotriene B4 (LTB4) was efficacious at causing loss of venular JAM-C and promoting neutrophil reverse transendothelial cell migration (rTEM) in vivo.
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A monoclonal antibody recognizing very late activation antigen-4 inhibits eosinophil accumulation in vivo.

TL;DR: A role for VLA-4 in eosinophil accumulation in vivo is suggested and a dissociation between the inflammatory events of eos inophils accumulation and edema formation is indicated.
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Matrix Metalloproteinase-9 Deficiency Results in Enhanced Allergen-Induced Airway Inflammation

TL;DR: The results indicate that M MP-9 is critically involved in the recruitment of eosinophils and Th2 cells to the lung following allergen challenge, and suggest that MMP-9 plays a role in the development of Th2 responses to allergan.
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Transmigration through venular walls: a key regulator of leukocyte phenotype and function.

TL;DR: The characteristics, potential mechanisms and the relevance of transmigration-induced change in leukocyte phenotype and responsiveness both within physiological and pathological scenarios are discussed.