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Eleni Douni

Researcher at Agricultural University of Athens

Publications -  56
Citations -  3555

Eleni Douni is an academic researcher from Agricultural University of Athens. The author has contributed to research in topics: Tumor necrosis factor alpha & RANKL. The author has an hindex of 23, co-authored 47 publications receiving 3188 citations. Previous affiliations of Eleni Douni include Pasteur Institute & Alexander Fleming Biomedical Sciences Research Center.

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The transmembrane form of tumor necrosis factor is the prime activating ligand of the 80 kda tumor necrosis factor receptor

TL;DR: It is shown here that the transmembrane form of TNF is superior to soluble TNF in activating TNFR80 in activating TNF-induced cellular responses in various systems such as T cell activation, thymocyte proliferation, and granulocyte/macrophage colony-stimulating factor production.
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On the role of tumor necrosis factor and receptors in models of multiorgan failure, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease.

TL;DR: Diverse functions of TNF/TNFRs are placed into context with the development of specific pathology in murine models of multiorgan failure, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease to suggest that TNF may also directly promote or downregulate the adaptive immune response.
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The function of tumour necrosis factor and receptors in models of multi-organ inflammation, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease.

TL;DR: The potential pathogenic mechanisms exerted by TNF and receptors in models of multi-organ inflammation, rheumatoid arthritis, multiple sclerosis and inflammatory bowel disease are discussed and the nature and level of contribution of these mechanisms in chronic inflammation and autoimmunity may lead to better regulatory and therapeutic applications.
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In vivo evidence for a functional role of both tumor necrosis factor (TNF) receptors and transmembrane TNF in experimental hepatitis.

TL;DR: It is demonstrated that a cooperation of TNFR1 and TNFR2 is required for hepatotoxicity as mice deficient of either receptor were resistant against Con A and transmembrane TNF is sufficient to mediate hepatic damage.
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RANKL inhibition improves muscle strength and insulin sensitivity and restores bone mass

TL;DR: In conclusions, RANKL deteriorates, while its inhibitor improves, muscle strength and insulin sensitivity in osteoporotic mice and humans, and denosumab could represent a novel therapeutic approach for sarcopenia.