M
M. Nain
Researcher at University of Marburg
Publications - 27
Citations - 2279
M. Nain is an academic researcher from University of Marburg. The author has contributed to research in topics: Influenza A virus & Tumor necrosis factor alpha. The author has an hindex of 21, co-authored 27 publications receiving 2204 citations.
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Journal Article
Release of tumor necrosis factor-alpha from macrophages. Enhancement and suppression are dose-dependently regulated by prostaglandin E2 and cyclic nucleotides.
TL;DR: Findings demonstrate that TNF-alpha synthesis in macrophages is up-regulated by cGMP and down- regulated by cAMP, which indicates that cyclic nucleotides act as intracellular messengers for extracellular signals of macrophage activation.
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Enhanced release of cytokines, interleukin-2 receptors, and neopterin after long-distance running
TL;DR: It is shown that long-distance running elevates cytokine production which supports the concept that regular, but not excessive, physical exercise may be beneficial by maintaining a stimulated immune system.
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Programmed Cell Death (Apoptosis) in Human Monocytes Infected by Influenza A Virus
TL;DR: It is demonstrated that influenza A virus-induced monocyte killing was due to programmed cell death (apoptosis) and not to necrosis, and damaging and inflammation-inducing lysosomal enzymes are held back from monocytes undergoing controlled cell death.
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Nucleic Acid-Sensing Toll-like Receptors Are Essential for the Control of Endogenous Retrovirus Viremia and ERV-Induced Tumors
Philipp Yu,Wolger Lübben,Heike Slomka,Janine Gebler,Madlen Konert,Chengcong Cai,Luisa Neubrandt,Olivia Prazeres da Costa,Stephanie Paul,Sonja Dehnert,Karolin Döhne,Michael Thanisch,Silke Storsberg,Lisa Wiegand,Andreas Kaufmann,M. Nain,Leticia Quintanilla-Martinez,Sabrina Bettio,Barbara S. Schnierle,Larissa Kolesnikova,Stephan Becker,Markus Schnare,Stefan Bauer +22 more
TL;DR: It is suggested that in addition to their role in innate immunity against exogenous pathogens, nucleic acid-recognizing Toll-like receptors 3, 7, and 9 contribute to the immune control of activated ERVs and ERV-induced tumors.
Journal Article
Macrophage activation by granulocyte/macrophage colony-stimulating factor. Priming for enhanced release of tumor necrosis factor-alpha and prostaglandin E2.
TL;DR: Data show that GM-CSF is capable of priming for the enhanced release of two factors, initially for TNF-alpha and subsequently for PGE2, which suggests an autoregulatory circuit in which the later produced P GE2 limits GM- CSF-induced macrophage activation.