scispace - formally typeset
A

Alma Zernecke

Researcher at University of Würzburg

Publications -  137
Citations -  8547

Alma Zernecke is an academic researcher from University of Würzburg. The author has contributed to research in topics: Inflammation & Chemokine. The author has an hindex of 47, co-authored 137 publications receiving 6986 citations. Previous affiliations of Alma Zernecke include Technische Universität München & Ludwig Maximilian University of Munich.

Papers
More filters
Journal ArticleDOI

JAM-1 is a ligand of the beta(2) integrin LFA-1 involved in transendothelial migration of leukocytes.

TL;DR: JAM-1 is a counter-receptor for LFA-1 that is ideally situated to guide and control transmigration during leukocyte recruitment and is also a ligand of the β2 integrin lymphocyte function–associated antigen 1.
Journal ArticleDOI

Single-Cell RNA-Seq Reveals the Transcriptional Landscape and Heterogeneity of Aortic Macrophages in Murine Atherosclerosis

TL;DR: Single-cell RNA sequencing unprecedentedly uncovered the transcriptional landscape and phenotypic heterogeneity of aortic macrophages and monocyte-derived dendritic cells in atherosclerotic arteries and identified previously unrecognized macrophage populations and their gene expression signature, suggesting specialized functions.
Journal ArticleDOI

Platelet Microparticles: A Transcellular Delivery System for RANTES Promoting Monocyte Recruitment on Endothelium

TL;DR: Circulating PMPs may serve as a finely tuned transcellular delivery system for RANTES, triggering monocyte arrest to inflamed and Atherosclerotic endothelium, introducing a novel mechanism for platelet-dependent monocyte recruitment in inflammation and atherosclerosis.
Journal ArticleDOI

Auto-Antigenic Protein-DNA Complexes Stimulate Plasmacytoid Dendritic Cells to Promote Atherosclerosis

TL;DR: Self-DNA released from dying cells or in neutrophil extracellular traps and an increased expression of the antimicrobial peptide Cramp/LL37 in atherosclerotic lesions may stimulate a pDC-driven pathway of autoimmune activation and the generation of anti–double-stranded-DNA antibodies, critically aggravating atherosclerosis lesion formation.