About: Stefan Lienenklaus

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An Entity of Type : wikibase:Item, within Data Space : wikidata.demo.openlinksw.com associated with source document(s)

researcher

Attributes	Values
rdf:type	Item
description	forskare (sv) researcher (en) 연구원 (ko) ricercatore (it) গবেষক (bn) 研究者 (ja) ഗവേഷകൻ (ml) araştırmacı (tr) wetenschapper (nl) дослідник (uk) эрдэмтэн (mn) изилдөөчү (ky) 研究者 (zh) հետազոտող (hy) hulumtues (sq)
rdfs:label	Stefan Lienenklaus (en) Stefan Lienenklaus (es) Stefan Lienenklaus (fr) Stefan Lienenklaus (nl) Stefan Lienenklaus (sl) Stefan Lienenklaus (tr) Stefan Lienenklaus (ast)
skos:prefLabel	Stefan Lienenklaus (en) Stefan Lienenklaus (es) Stefan Lienenklaus (fr) Stefan Lienenklaus (nl) Stefan Lienenklaus (sl) Stefan Lienenklaus (tr) Stefan Lienenklaus (ast)
name	Stefan Lienenklaus (en) Stefan Lienenklaus (es) Stefan Lienenklaus (fr) Stefan Lienenklaus (nl) Stefan Lienenklaus (sl) Stefan Lienenklaus (tr) Stefan Lienenklaus (ast)
Scopus author ID	wds:Q41582017-46F8B53D-1446-4525-A637-DB44B80684AD
Scopus author ID	6505895085
given name	wds:Q41582017-B183A547-DAC0-4445-A769-CDAA1E641246
given name	Stefan
instance of	wds:Q41582017-C64B696C-2B01-4016-B287-781EC73CBB5A
instance of	Homo sapiens
occupation	wds:Q41582017-EA80650A-EFDB-4FDB-A4C5-99AF357A9183
employer	wds:Q41582017-96B39899-ED03-4782-8906-D1BCC2B4DE58 wds:Q41582017-A05F0EBB-E05A-4A53-A703-5BC7A3A5C0F8 wds:Q41582017-A335767C-A9A9-444F-AA9A-C552AA2B3224
sex or gender	wds:Q41582017-77B4AC2A-9A86-466A-BD68-5AF213C55D76
VIAF ID	wds:Q41582017-5394DAF4-D101-4EFD-ADC7-97C69B646A8D
GND ID	wds:Q41582017-fa1d9af0-9d2b-49aa-a934-b5b4e34726df
WorldCat Identities ID (superseded)	wds:Q41582017-7C7014B8-F754-4814-8681-C294977849A4
VIAF ID	http://viaf.org/viaf/67386154
GND ID	https://d-nb.info/gnd/123926513
occupation	researcher
employer	Hannover Medical School Helmholtz Centre for Infection Research Center for Experimental and Clinical Infection Research
sex or gender	male
VIAF ID	67386154
GND ID	123926513
WorldCat Identities ID (superseded)	viaf-67386154
ORCID iD	wds:Q41582017-EC50D6E5-E6AB-4DC4-8454-AC675F1C8C3F
ORCID iD	https://orcid.org/0000-0003-4790-3445
ORCID iD	0000-0003-4790-3445
is about of	https://www.wikidata.org/wiki/Special:EntityData/Q41582017
is author of	Novel reporter mouse reveals constitutive and inflammatory expression of IFN-beta in vivo Temporal and spatial resolution of type I and III interferon responses in vivo Conditional IFNAR1 ablation reveals distinct requirements of Type I IFN signaling for NK cell maturation and tumor surveillance Lack of interferon-beta leads to accelerated remyelination in a toxic model of central nervous system demyelination DNA damage primes the type I interferon system via the cytosolic DNA sensor STING to promote anti-microbial innate immunity Neutrophils responsive to endogenous IFN-beta regulate tumor angiogenesis and growth in a mouse tumor model The lack of type I interferon induces neutrophil-mediated pre-metastatic niche formation in the mouse lung. Delayed apoptosis of tumor associated neutrophils in the absence of endogenous IFN-β. Priming of natural killer cells by nonmucosal mononuclear phagocytes requires instructive signals from commensal microbiota. Reversible silencing of cytomegalovirus genomes by type I interferon governs virus latency. Tumor invasion of Salmonella enterica serovar Typhimurium is accompanied by strong hemorrhage promoted by TNF-alpha Hepatitis C virus replication in mouse cells is restricted by IFN-dependent and -independent mechanisms Type I interferon drives tumor necrosis factor-induced lethal shock Glycine 184 in nonstructural protein NS1 determines the virulence of influenza A virus strain PR8 without affecting the host interferon response Mouse SAMHD1 has antiretroviral activity and suppresses a spontaneous cell-intrinsic antiviral response Murine toll-like receptor 2 activation induces type I interferon responses from endolysosomal compartments Visualizing the beta interferon response in mice during infection with influenza A viruses expressing or lacking nonstructural protein 1. Norovirus triggered microbiota-driven mucosal inflammation in interleukin 10-deficient mice Induction of B-cell development in adult mice reveals the ability of bone marrow to produce B-1a cells. Signals triggered by a bacterial pore-forming toxin contribute to toll-like receptor redundancy in gram-positive bacterial recognition Production of IFN-β during Listeria monocytogenes infection is restricted to monocyte/macrophage lineage Type I Interferon Signaling Prevents IL-1β-Driven Lethal Systemic Hyperinflammation during Invasive Bacterial Infection of Soft Tissue. M27 expressed by cytomegalovirus counteracts effective type I interferon induction of myeloid cells but not of plasmacytoid dendritic cells Induction of endogenous Type I interferon within the central nervous system plays a protective role in experimental autoimmune encephalomyelitis. RIG-I/MAVS and STING signaling promote gut integrity during irradiation- and immune-mediated tissue injury Transformation of mouse fibroblasts alters the induction pattern of type I IFNs after virus infection TLR7 contributes to the rapid progression but not to the overall fatal outcome of secondary pneumococcal disease following influenza A virus infection. Strong interferon-inducing capacity of a highly virulent variant of influenza A virus strain PR8 with deletions in the NS1 gene Immunoglobulins drive terminal maturation of splenic dendritic cells. In Vivo Visualizing the IFN-β Response Required for Tumor Growth Control in a Therapeutic Model of Polyadenylic-Polyuridylic Acid Administration. Upon intranasal vesicular stomatitis virus infection, astrocytes in the olfactory bulb are important interferon Beta producers that protect from lethal encephalitis Age-dependent enterocyte invasion and microcolony formation by Salmonella Influence of internalin A murinisation on host resistance to orally acquired listeriosis in mice. Genetic models reveal origin, persistence and non-redundant functions of IL-17-producing γδ T cells Type I interferon protects mice from fatal neurotropic infection with Langat virus by systemic and local antiviral responses.

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