Zobrazeno 1 - 10
of 17
pro vyhledávání: '"Ingmar A F M, Heijnen"'
Autor:
Pascal Urwyler, Marina Leimbacher, Panteleimon Charitos, Stephan Moser, Ingmar A. F. M. Heijnen, Marten Trendelenburg, Reto Thoma, Johannes Sumer, Adrián Camacho-Ortiz, Marcelo R. Bacci, Lars C. Huber, Melina Stüssi-Helbling, Werner C. Albrich, Parham Sendi, Michael Osthoff
Publikováno v:
Frontiers in Immunology, Vol 14 (2023)
BackgroundConestat alfa (ConA), a recombinant human C1 inhibitor, may prevent thromboinflammation.MethodsWe conducted a randomized, open-label, multi-national clinical trial in which hospitalized adults at risk for progression to severe COVID-19 were
Externí odkaz:
https://doaj.org/article/13e39c08209c4b4b9e955d59ae6dbb21
Autor:
Panteleimon Charitos, Ingmar A. F. M. Heijnen, Adrian Egli, Stefano Bassetti, Marten Trendelenburg, Michael Osthoff
Publikováno v:
Frontiers in Immunology, Vol 12 (2021)
AimsAlthough the exact factors promoting disease progression in COVID-19 are not fully elucidated, unregulated activation of the complement system (CS) seems to play a crucial role in the pathogenesis of acute lung injury (ALI) induced by SARS-CoV-2.
Externí odkaz:
https://doaj.org/article/1cdfa175ee6b44ce863c0bacb6533711
Autor:
Pascal Urwyler, Panteleimon Charitos, Stephan Moser, Ingmar A. F. M. Heijnen, Marten Trendelenburg, Reto Thoma, Johannes Sumer, Adrián Camacho-Ortiz, Marcelo R. Bacci, Lars C. Huber, Melina Stüssi-Helbling, Werner C. Albrich, Parham Sendi, Michael Osthoff
Publikováno v:
Trials, Vol 22, Iss 1, Pp 1-3 (2021)
Abstract Objectives Conestat alfa, a recombinant human C1 esterase inhibitor, is a multi-target inhibitor of inflammatory cascades including the complement, the kinin-kallikrein and the contact activation system. The study objective is to investigate
Externí odkaz:
https://doaj.org/article/94b47821094d40348464c6a01a92f215
Autor:
Michael Osthoff, Veronika K. Jaeger, Ingmar A. F. M. Heijnen, Marten Trendelenburg, Suzana Jordan, Oliver Distler, Ulrich A. Walker
Publikováno v:
Arthritis Research & Therapy, Vol 21, Iss 1, Pp 1-8 (2019)
Abstract Background The role of the complement system in the pathogenesis of systemic sclerosis (SSc) is controversial. This study investigated the role of the lectin pathway of complement as a mediator of ischemia/reperfusion injury in SSc. Methods
Externí odkaz:
https://doaj.org/article/5d280bb03cd84b4884c3e66225c39709
Autor:
Philipp S. Fuchs, Jonas Lötscher, Caroline M. Berkemeier, Julia R. Hirsiger, Adhideb Ghosh, Quan-Zhen Li, Nikolaus Deigendesch, Emanuel Christ, Alexander A. Navarini, Mike Recher, Thomas Daikeler, Ingmar A. F. M. Heijnen, Christoph T. Berger
Publikováno v:
Frontiers in Immunology, Vol 11 (2020)
BackgroundANCA-associated vasculitis (AAV) and Sjögren’s syndrome (SS) are uncommon autoimmune diseases. The co-occurrence in the same patient has been rarely described. Acromegaly has been associated with autoimmune thyroiditis, but the prevalenc
Externí odkaz:
https://doaj.org/article/519ffe4a909d4784ab512654423d8dfd
Autor:
Pascal Urwyler, Stephan Moser, Panteleimon Charitos, Ingmar A. F. M. Heijnen, Melanie Rudin, Gregor Sommer, Bruno M. Giannetti, Stefano Bassetti, Parham Sendi, Marten Trendelenburg, Michael Osthoff
Publikováno v:
Frontiers in Immunology, Vol 11 (2020)
A dysregulated immune response with hyperinflammation is observed in patients with severe coronavirus disease 2019 (COVID-19). The aim of the present study was to assess the safety and potential benefits of human recombinant C1 esterase inhibitor (co
Externí odkaz:
https://doaj.org/article/73299d9df6f94090a0e9e649115d6273
Autor:
Jamie Honeychurch, Alison L. Tutt, Thomas Valerius, Ingmar A. F. M. Heijnen, Jan G. J. Van de Winkel, Martin J. Glennie
Publikováno v:
Blood. 96:3544-3552
CD64 (FcγRI) receptors represent highly potent trigger molecules for activated polymorphonuclear cells (PMN) and mediate lysis of a range of tumors in the presence of appropriate monoclonal antibodies. An huCD64 transgenic mouse model designed to an
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::01b2a2d9474cf8a802b9889aa012dab6
https://doi.org/10.1182/blood.v96.10.3544.h8003544_3544_3552
https://doi.org/10.1182/blood.v96.10.3544.h8003544_3544_3552
Autor:
Wouter L. W. Hazenbos, Ingmar A. F. M. Heijnen, Dirk Meyer, Frans M. A. Hofhuis, Chantal Renardel de Lavalette, Reinhold E. Schmidt, Peter J. A. Capel, Jan G. J. van de Winkel, J. Engelbert Gessner, Timo K. van den Berg, J. Sjef Verbeek
Publikováno v:
The Journal of Immunology. 161:3026-3032
Previously, we have demonstrated that phagocytosis of IgG1-coated particles by macrophages in vitro is impaired by deletion of FcγRIII in mice, suggesting that IgG1 may interact preferentially with FcγRIII. In the present study, the biologic releva
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::6ca197a68ce28ae62b841027f96a47bc
https://doi.org/10.4049/jimmunol.161.6.3026
https://doi.org/10.4049/jimmunol.161.6.3026
Publikováno v:
Cancer Immunology, Immunotherapy. 45:166-170
The class I IgG receptor (Fc gamma RI) on cytotoxic effector cells has been reported to initiate destruction of tumour cells by effector cells in vitro. We are aiming at developing an immunocompetent model to evaluate the cytotoxic capacity of human
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::37087e9ba8cd2b201a6e68fc7f06bef7
https://doi.org/10.1007/s002620050424
https://doi.org/10.1007/s002620050424
Autor:
Ingmar A F M, Heijnen, C, Foocharoen, Bettina, Bannert, Patricia E, Carreira, Roberto, Caporali, Vanessa, Smith, Gábor, Kumánovics, Mike O, Becker, Marie, Vanthuyne, Ismail, Simsek, Chiara, Bocelli-Tyndall, Ulrich A, Walker
Publikováno v:
Clinical and experimental rheumatology. 31(2 Suppl 76)
To determine the clinical characteristics of simultaneous occurrence of antitopoisomerase (ATA) and anticentromere (ACA) autoantibodies in systemic sclerosis (SSc).Data of patients (n=4,687) fulfilling the ACR criteria for SSc and followed in the EUL
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::789b00d9a91bc98e8c29f6dea8840226
https://pubmed.ncbi.nlm.nih.gov/23101460
https://pubmed.ncbi.nlm.nih.gov/23101460