![]() | Thomas Anton LugerShow email addressClinic for Dermatology, University Hospital Münster, Münster, Germany | Department of Dermatology, University Hospital Münster, University Muenster, Von Esmarchstrasse 58, ... |
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Thomas Anton Luger:Expert Impact
Concepts for whichThomas Anton Lugerhas direct influence:Atopic dermatitis,Chronic pruritus,Pimecrolimus cream.
Thomas Anton Luger:KOL impact
Concepts related to the work of other authors for whichfor which Thomas Anton Luger has influence:Atopic dermatitis,Psoriatic arthritis,Mast cells,Human keratinocytes,Chronic pruritus,Necrosis factor,Gene expression.
KOL Resume for Thomas Anton Luger
Year | |
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2022 | Clinic for Dermatology, University Hospital Münster, Münster, Germany |
2021 | Department of Dermatology, University Hospital Münster, Münster, Germany |
2019 | Department of Dermatology, University Hospital of Muenster, Muenster, Germany |
2018 | Department of Dermatology, Laboratory for Neuroendocrinology of the Skin and Interdisciplinary Endocrinology, University of Münster, Von Esmarch‐Str. 58, 48149, Münster, Germany Klinik für Hautkrankheiten, Universitätsklinikum Münster, Münster, Deutschland |
2017 | Universitätsklinikum Münster Klinik für Hautkrankheiten Münster |
2016 | Department of Dermatology, University of Münster, Münster (T.L.), and SCIderm Research Institute and Dermatologikum Hamburg, Hamburg (K.R.) — both in Germany Klinik für Hautkrankheiten, Allgemeine Dermatologie und Venerologie Universitätsklinikum Münster Deutschland |
2015 | Department of Dermatology, University Hospital Münster, Münster, Germany. Universitätsklinikum Münster Klinik für Hautkrankheiten – Allgemeine Dermatologie und Venerologie University Hospital of Münster, Von-Esmarch-Strasse 58, 48149, Münster, Germany |
2014 | Interdisciplinary Center of Clinical Research Münster Department of Dermatology, University of Muenster, Germany |
2013 | Department of Dermatology Kompetenzzentrum Chronischer Pruritus (KCP), Klinik für Hautkrankheiten, Universitätsklinikum Münster, Von-Esmarch-Str. 58, 48149, Münster, Deutschland |
2012 | Department of Dermatology, Competence Center Chronic Pruritus, University Hospital of Münster, Münster, Germany Klinik und Poliklinik für Hautkrankheiten, Universitätsklinikum Münster, Münster |
2011 | Clinic and Polyclinic for Dermatological Diseases, Münster University Hospital, Germany Kompetenzzentrum Chronischer Pruritus, Klinik und Poliklinik für Hautkrankheiten, Universitätsklinikum Münster TA Luger Departments of Dermatology |
2010 | Interdisciplinary Center of Clinical Research, University of Münster, Münster, Germany Department of Dermatology, University of Münster, Münster; Klinik und Poliklinik für Hautkrankheiten – Allgemeine Dermatologie und Venerologie, Universitätsklinikum Münster, Von-Esmarch-Str. 58, 48149, Münster, Deutschland |
2009 | Klinik und Polyklinik für Hautkrankheiten, Von‐Esmarch‐Strasse 58, 48149 Münster (Germany) Department of Dermatology, University of Münster, Von‐Esmarch‐Str. 58, 48149 Münster, Germany |
Concept | World rank |
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human normal serum | #1 |
human skin psoriasis | #1 |
nonmelanocytic cell types | #1 |
skin immune systems | #1 |
a375 cell mrna | #1 |
300 efficacy | #1 |
neoplastic humans cytokine | #1 |
melanocortin corticotropinreleasing hormone | #1 |
human keratinocytes regulation | #1 |
human dpcs alphamsh | #1 |
ncas bgp | #1 |
par2 cutaneous inflammation | #1 |
nk1r acd | #1 |
mora treatment | #1 |
tcis infants | #1 |
clasi acle | #1 |
ca2 camp assays | #1 |
putative neuronal mechanisms | #1 |
atopic humans pimecrolimus | #1 |
systemic administration tacrolimus | #1 |
situ human sebocytes | #1 |
iddm basal conditions | #1 |
melanocortin analogue nle4‐d‐phe7‐α‐msh | #1 |
protection uvinduced immunosuppression | #1 |
articular rtpcr | #1 |
illness aged allergens | #1 |
puva versus | #1 |
damage subtypes | #1 |
hormones humans inflammation | #1 |
28 56 84 | #1 |
resultsa therapeutic response | #1 |
year skin diseases | #1 |
inflammation melanocortins melanocortin | #1 |
immune intercellular | #1 |
maintenance treatment flares | #1 |
alpha msh acth | #1 |
uvirradiated kc addition | #1 |
timing pruritus relief | #1 |
mc1rpositive basophils | #1 |
alphamsh fibroblastic cells | #1 |
32 dcl | #1 |
dpcs hair follicle | #1 |
qol isga | #1 |
differentiated hacat cells | #1 |
causion | #1 |
tacrolimus body locations | #1 |
vasointenstinal peptide | #1 |
uv light cd95 | #1 |
azathioprine complete remission | #1 |
dlqi sps score | #1 |
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Prominent publications by Thomas Anton Luger
BACKGROUND: Two phase 3 trials (UNCOVER-2 and UNCOVER-3) showed that at 12 weeks of treatment, ixekizumab, a monoclonal antibody against interleukin-17A, was superior to placebo and etanercept in the treatment of moderate-to-severe psoriasis. We report the 60-week data from the UNCOVER-2 and UNCOVER-3 trials, as well as 12-week and 60-week data from a third phase 3 trial, UNCOVER-1.
METHODS: We randomly assigned 1296 patients in the UNCOVER-1 trial, 1224 patients in the UNCOVER-2 trial, ...
Known for 3 Trials | Ixekizumab Placebo | Week Patients | Spga Score | Starting Dose |
Intercellular adhesion molecule-1 (ICAM-1) is involved in cell-cell interactions of leukocytes and parenchymal cells and thus plays an important role in immunologic and inflammatory reactions. The expression of ICAM-1 that is found on many different cells such as melanocytes and melanoma cells is induced by various cytokines, including interferon-gamma (IFN gamma), interleukin (IL)-1 and tumor necrosis factor alpha (TNF alpha). Because expression of ICAM-1 in melanoma was found to ...
Known for Melanoma Cells | Intercellular Adhesion | Icam1 Expression | Tnf Alpha | Human Melanocytes |
Irradiation with ultraviolet (UV) B radiation results in the formation of apoptotic keratinocytes called sunburn cells. Recently, it was demonstrated that keratinocytes can release tumor necrosis factor-alpha (TNF-alpha), which is known to cause apoptosis in particular cells. In addition, it has been shown that UVB light induces the release of TNF-alpha by keratinocytes and that keratinocytes express the 55-kD receptor for TNF-alpha. Therefore, we investigated whether TNF-alpha is ...
Known for Sunburn Cells | Induced Apoptosis | Tumor Necrosis | Tnfalpha Keratinocytes | Alpha Tnf |
BACKGROUND: In previous studies, etanercept 25 mg twice weekly (BIW) or 50 mg BIW significantly reduced disease severity in patients with plaque psoriasis and demonstrated a favourable safety profile.
OBJECTIVES: To assess the efficacy and safety of etanercept 50 mg administered once weekly (QW) compared with placebo in patients with moderate-to-severe plaque psoriasis over 24 weeks.
METHODS: This study was conducted in two parts: (i) a 12-week, double-blind, placebo-controlled phase, in ...
Known for Etanercept 50 | Plaque Psoriasis | Week Patients | Placebo Qw | Baseline Pasi |
BACKGROUND: Secukinumab, a fully human monoclonal antibody that selectively neutralizes IL-17A, has been shown to have significant efficacy and a favourable safety profile in the treatment of moderate-to-severe psoriasis and psoriatic arthritis.
OBJECTIVE: To assess the efficacy and safety of secukinumab through 5 years of treatment in moderate-to-severe psoriasis.
METHODS: In the core SCULPTURE study, Psoriasis Area and Severity Index (PASI) 75 responders at Week 12 continued receiving ...
Known for 5 Years | Extension Study | Monoclonal Antibodies | Favourable Safety | Sustained Efficacy |
BACKGROUND: Tofacitinib is an oral Janus kinase inhibitor being investigated for psoriasis.
OBJECTIVES: To determine the 16-week efficacy and safety of two oral tofacitinib doses vs. placebo in patients with moderate-to-severe chronic plaque psoriasis.
METHODS: Patients in two similarly designed phase III studies (OPT Pivotal 1, NCT01276639, n = 901; OPT Pivotal 2, NCT01309737, n = 960) were initially randomized 2 : 2 : 1 to tofacitinib 10 or 5 mg or placebo, twice daily. Coprimary ...
Known for Tofacitinib Placebo | Opt Pivotal | Plaque Psoriasis | Phase Iii | Oral Janus |
Corticotropin Releasing Hormone and Proopiomelanocortin Involvement in the Cutaneous Response to Stress
[ PUBLICATION ]
The skin is a known target organ for the proopiomelanocortin (POMC)-derived neuropeptides alpha-melanocyte stimulating hormone (alpha-MSH), beta-endorphin, and ACTH and also a source of these peptides. Skin expression levels of the POMC gene and POMC/corticotropin releasing hormone (CRH) peptides are not static but are determined by such factors as the physiological changes associated with hair cycle (highest in anagen phase), ultraviolet radiation (UVR) exposure, immune cytokine ...
Known for Corticotropin Releasing | Pomc Peptides | Cutaneous Response | Skin Expression | Hormone Receptors |
Ultraviolet Light Induces Apoptosis via Direct Activation of CD95 (Fas/APO-1) Independently of Its Ligand CD95L
[ PUBLICATION ]
Induction of apoptosis in keratinocytes by UV light is a critical event in photocarcinogenesis. Although p53 is of importance in this process, evidence exists that other pathways play a role as well. Therefore, we studied whether the apoptosis-related surface molecule CD95 (Fas/APO-1) is involved. The human keratinocyte cell line HaCaT expresses CD95 and undergoes apoptosis after treatment with UV light or with the ligand of CD95 (CD95L). Incubation with a neutralizing CD95 antibody ...
Known for Uv Light | Direct Activation | Ligand Cd95 | Induces Apoptosis | Recruitment Fadd |
Tumor necrosis factor-related apoptosis-inducing ligand (TRAIL), a new member of the tumor necrosis factor (TNF) family, induces apoptosis primarily of transformed cells. Interleukin-1 was previously found to protect the keratinocyte cell line KB from TRAIL-induced apoptosis, thus we studied whether interleukin-1 also protects from other apoptotic stimuli (ultraviolet radiation (UV), CD95-ligand). Interleukin-1 rescued KB cells from TRAIL- and CD95-induced apoptosis, which was critically ...
Known for Tumor Necrosis | Induced Apoptosis | Ultraviolet Radiation | Transformed Keratinocytes | Inducing Ligand |
BACKGROUND: Since the publication of the European League Against Rheumatism recommendations for the pharmacological treatment of psoriatic arthritis (PsA) in 2012, new evidence and new therapeutic agents have emerged. The objective was to update these recommendations.
METHODS: A systematic literature review was performed regarding pharmacological treatment in PsA. Subsequently, recommendations were formulated based on the evidence and the expert opinion of the 34 Task Force members. ...
Known for European League | Pharmacological Therapies | Psoriatic Arthritis | Recommendations Evidence | Overarching Principles |
Proteinase-activated receptor 2 belongs to a new G protein-coupled receptor subfamily activated by various serine proteases. It has been demonstrated to play a role during inflammation of many tissues including the skin. Proteinase-activated receptor 2 is expressed by endothelial cells and regulates cutaneous inflammation in vivo. The underlying mechanisms of proteinase-activated receptor 2 activation in the skin and the effects on human dermal microvascular endothelial cells, however, ...
Known for Endothelial Cells | Activated Receptor | Cutaneous Inflammation | Inflammatory Responses | Human Dermal |
OBJECTIVE: Recently, we found that human dermal fibroblasts (HDFs) express melanocortin 1 receptors (MC-1R) that bind alpha-melanocyte-stimulating hormone (alpha-MSH). In search of novel therapies for scleroderma (systemic sclerosis [SSc]), we used the bleomycin (BLM) model to investigate the effects of alpha-MSH on collagen synthesis and fibrosis.
METHODS: Collagen expression in HDFs was determined by real-time reverse transcription-polymerase chain reaction (RT-PCR) and Western blot ...
Known for Mouse Model | Tissue Fibrosis | Melanocortin Peptides | Stimulating Hormone | Messenger Receptors |
Pentoxifylline (PTX) is a methylxanthine compound known to inhibit the production of tumour necrosis factor-alpha (TNF-alpha), which is an important inflammatory mediator. There is also recent evidence that PTX may influence other inflammatory cytokines, such as interleukin-1 (IL-1) and IL-6. Due to the therapeutic implications, the present study addressed the in vivo effects of PTX on the release of TNF-alpha, IL-1 beta, IL-6 and IL-8 by human peripheral blood mononuclear cells (PBMC). ...
Known for Necrosis Factor | Mononuclear Cells | Pentoxifylline Ptx | Cytokine Release | Il1 Beta |