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Elsner J

Researcher at Fraunhofer Society

Publications -  7
Citations -  272

Elsner J is an academic researcher from Fraunhofer Society. The author has contributed to research in topics: Neutropenia & Congenital Neutropenia. The author has an hindex of 6, co-authored 7 publications receiving 263 citations. Previous affiliations of Elsner J include Hochschule Hannover.

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Functional features of neutrophils induced by G-CSF and GM-CSF treatment: differential effects and clinical implications

TL;DR: This review summarizes major functional and phenotypical features of neutrophils induced by G-CSF treatment in patients with acquired and congenital neutropenias and focuses on the differential effect of G- CSF and GM-SF on neutrophil function in vitro and in vivo.
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In vitro functions of neutrophils induced by treatment with rhG-CSF in severe congenital neutropenia.

TL;DR: Good clinical improvements of patients suffering from SCN after treatment with rh G‐CSF appeared to be due to induction of neutrophils displaying overall good functional activities with respect to natural defense.
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Altered function and surface marker expression of neutrophils induced by rhG-CSF treatment in severe congenital neutropenia

TL;DR: Data demonstrate that the decrease of chemotaxis of neutrophils from SCN patients is not due to a decrease in the number of intra‐ or extracellular FMLP receptors; however, the decreasedChemotaxis could result from an altered FMLP receptor turnover.
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Production of oxygen radicals by fibroblasts and neutrophils from a patient with x-linked chronic granulomatous disease.

TL;DR: Data demonstrate, in contrast to previous studies, that fibroblasts are able to produce ROI, and since fibro Blasts obtained from a CGD patient exhibited no difference in ROI production compared with fibroblast obtained from healthy donors, they are not suitable for prenatal diagnosis of CGD.
Journal Article

Abnormal regulation in the signal transduction in neutrophils from patients with severe congenital neutropenia: relation of impaired mobilization of cytosolic free calcium to altered chemotaxis, superoxide anion generation and F-actin content.

TL;DR: Data suggest a defect in the signal transduction pathway in neutrophils from SCN patients between FMLP ligand-receptor interaction and Ca2+ mobilization, whereas upstream of PKC, triggered events seem to be unaffected.