Margaret E. Walker
Northwestern University
6 Papers
23 Citations
Margaret E. Walker is an academic researcher from Northwestern University. The author has contributed to research in topics: Tumor necrosis factor alpha & Inflammation. The author has an hindex of 6, co-authored 6 publications.
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Papers
Meningeal mast cells affect early T cell central nervous system infiltration and blood-brain barrier integrity through TNF: a role for neutrophil recruitment?
TL;DR: It is proposed that neutrophils in turn promote the blood-brain barrier breach and together with T cells lead to further inflammatory cell influx and myelin damage, providing specific targets for intervention in multiple sclerosis as well as other immune-mediated CNS diseases.
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New insights into the role of mast cells in autoimmunity: evidence for a common mechanism of action?
TL;DR: The current state of knowledge about mast cells in autoimmune disease is reviewed and findings regarding newly discovered mast cell actions and factors that modulate mast cell function are discussed.
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Cutting Edge: Mast Cells Regulate Disease Severity in a Relapsing–Remitting Model of Multiple Sclerosis
TL;DR: It is confirmed that MC influence is not confined to an isolated model of EAE and revealed a new system to study the effects of MC heterogeneity on relapsing–remitting Eae and other SJL strain-specific diseases.
The Pla protease of Yersinia pestis degrades fas ligand to manipulate host cell death and inflammation.
TL;DR: It is shown that Pla degrades the apoptotic signaling molecule Fas ligand (FasL) to prevent host cell apoptosis and inflammation, and that Δpla infection results in aberrant proinflammatory cytokine levels.
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Genetic determination of essential residues of the Vibrio cholerae actin cross-linking domain reveals functional similarity with glutamine synthetases
Brett Geissler,Amanda Bonebrake,Amanda Bonebrake,Kerri Lynn Sheahan,Kerri Lynn Sheahan,Margaret E. Walker,Karla J. F. Satchell +6 more
TL;DR: It was determined that several residues demonstrated to be important for ACDVc activity are conserved with active‐site residues of the glutamine synthetase family of enzymes, indicating that the ACDs are a family of bacterial toxin effectors that may be evolutionarily related to ligases involved in amino acid biosynthesis.
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