scispace - formally typeset
F

Frederick J. Schnell

Researcher at Emory University

Publications -  14
Citations -  1980

Frederick J. Schnell is an academic researcher from Emory University. The author has contributed to research in topics: T cell & Cell junction. The author has an hindex of 12, co-authored 14 publications receiving 1877 citations. Previous affiliations of Frederick J. Schnell include Montana State University & Brigham and Women's Hospital.

Papers
More filters
Journal ArticleDOI

Junction Adhesion Molecule Is a Receptor for Reovirus

TL;DR: Reovirus interaction with cell-surface receptors is a critical determinant of both cell-type specific tropism and virus-induced intracellular signaling events that culminate in cell death.
Journal ArticleDOI

Human junction adhesion molecule regulates tight junction resealing in epithelia.

TL;DR: It is suggested that JAM plays an important role in the regulation of tight junction assembly in epithelia, and these JAM-mediated effects may occur by either direct, or indirect interactions with occludin.
Journal ArticleDOI

Signal Regulatory Protein (SIRPα), a Cellular Ligand for CD47, Regulates Neutrophil Transmigration

TL;DR: It is shown that SirPα1 directly binds to the immunoglobulin variable domain loop of purified human CD47 and that such SIRP-CD47 interactions regulate PMN transmigration, demonstrating that PMN migration is regulated by CD47 through SIRpα-dependent and SIRFα-independent mechanisms.
Journal ArticleDOI

Reduced Expression of Junctional Adhesion Molecule and Platelet/Endothelial Cell Adhesion Molecule-1 (CD31) at Human Vascular Endothelial Junctions by Cytokines Tumor Necrosis Factor-α Plus Interferon-γ Does Not Reduce Leukocyte Transmigration Under Flow

TL;DR: Results confirm that culture of human umbilical vein endothelial cells with TNF-alpha plus IFN-gamma caused a decrease in surface-expressed and junctional-localized JAM and PECAM-1, but did not cause decreased leukocyte transmigration in an in vitro flow assay, suggesting lack of correlation between transmigration and loss of permeability.
Journal ArticleDOI

An IL-7-dependent rebound in thymic T cell output contributes to the bone loss induced by estrogen deficiency.

TL;DR: It is concluded that IL-7 is a pivotal upstream target through which estrogen regulates hematopoietic and immune functions that are critical for bone homeostasis and due to both the thymic and extrathymic mechanisms.