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Your search keyword '"Kölsch, Uwe"' showing total 14 results
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14 results on '"Kölsch, Uwe"'

2. Variants in IGLL1 cause a broad phenotype from agammaglobulinemia to transient hypogammaglobulinemia

Author

Soomann, Maarja, Bily, Viktor, Elgizouli, Magdeldin, Kraemer, Dennis, Akgül, Gülfirde, von Bernuth, Horst, Bloomfield, Markéta, Brodszki, Nicholas, Candotti, Fabio, Förster-Waldl, Elisabeth, Freiberger, Tomas, Giżewska, Maria, Klocperk, Adam, Kölsch, Uwe, Nichols, Kim E., Krüger, Renate, Oak, Ninad, Pac, Małgorzata, Prader, Seraina, Schmiegelow, Kjeld, Šedivá, Anna, Sogkas, Georgios, Stittrich, Anna, Stoltze, Ulrik Kristoffer, Theodoropoulou, Katerina, Wadt, Karin, Wong, Melanie, Zeyda, Maximillian, Pachlopnik Schmid, Jana, and Trück, Johannes

Published
2024
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3. Screening Newborns for Low T Cell Receptor Excision Circles (TRECs) Fails to Detect Immunodeficiency, Centromeric Instability, and Facial Anomalies Syndrome

Author

Staudacher, Olga, Klein, Jeanette, Thee, Stephanie, Ullrich, Jan, Wahn, Volker, Unterwalder, Nadine, Kölsch, Uwe, Lankes, Erwin, Stittrich, Anna, Dedieu, Cinzia, Dinges, Sarah, Völler, Mirjam, Schuetz, Catharina, Schulte, Johannes, Boztug, Kaan, Meisel, Christian, Kuehl, Jörn-Sven, Krüger, Renate, Blankenstein, Oliver, and von Bernuth, Horst

Published
2023
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5. Early and Rapid Identification of COVID-19 Patients with Neutralizing Type I Interferon Auto-antibodies

Author

Akbil, Bengisu, Meyer, Tim, Stubbemann, Paula, Thibeault, Charlotte, Staudacher, Olga, Niemeyer, Daniela, Jansen, Jenny, Mühlemann, Barbara, Doehn, Jan, Tabeling, Christoph, Nusshag, Christian, Hirzel, Cédric, Sanchez, David Sökler, Nieters, Alexandra, Lother, Achim, Duerschmied, Daniel, Schallner, Nils, Lieberum, Jan Nikolaus, August, Dietrich, Rieg, Siegbert, Falcone, Valeria, Hengel, Hartmut, Kölsch, Uwe, Unterwalder, Nadine, Hübner, Ralf-Harto, Jones, Terry C., Suttorp, Norbert, Drosten, Christian, Warnatz, Klaus, Spinetti, Thibaud, Schefold, Joerg C., Dörner, Thomas, Sander, Leif Erik, Corman, Victor M., Merle, Uta, Kurth, Florian, von Bernuth, Horst, Meisel, Christian, and Goffinet, Christine

Published
2022
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6. Untimely TGFβ responses in COVID-19 limit antiviral functions of NK cells

Author

Witkowski, Mario, Tizian, Caroline, Ferreira-Gomes, Marta, Niemeyer, Daniela, Jones, Terry C., Heinrich, Frederik, Frischbutter, Stefan, Angermair, Stefan, Hohnstein, Thordis, Mattiola, Irene, Nawrath, Philipp, McEwen, Sophie, Zocche, Silvia, Viviano, Edoardo, Heinz, Gitta Anne, Maurer, Marcus, Kölsch, Uwe, Chua, Robert Lorenz, Aschman, Tom, Meisel, Christian, Radke, Josefine, Sawitzki, Birgit, Roehmel, Jobst, Allers, Kristina, Moos, Verena, Schneider, Thomas, Hanitsch, Leif, Mall, Marcus A., Conrad, Christian, Radbruch, Helena, Duerr, Claudia U., Trapani, Joseph A., Marcenaro, Emanuela, Kallinich, Tilmann, Corman, Victor M., Kurth, Florian, Sander, Leif Erik, Drosten, Christian, Treskatsch, Sascha, Durek, Pawel, Kruglov, Andrey, Radbruch, Andreas, Mashreghi, Mir-Farzin, and Diefenbach, Andreas

Published
2021
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7. The spinal cord injury-induced immune deficiency syndrome: results of the SCIentinel study

Author

Kopp, Marcel A, primary, Meisel, Christian, additional, Liebscher, Thomas, additional, Watzlawick, Ralf, additional, Cinelli, Paolo, additional, Schweizerhof, Oliver, additional, Blex, Christian, additional, Lübstorf, Tom, additional, Prilipp, Erik, additional, Niedeggen, Andreas, additional, Druschel, Claudia, additional, Schaser, Klaus-Dieter, additional, Wanner, Guido A, additional, Curt, Armin, additional, Lindemann, Gertraut, additional, Nugeva, Natalia, additional, Fehlings, Michael G, additional, Vajkoczy, Peter, additional, Cabraja, Mario, additional, Dengler, Julius, additional, Ertel, Wolfgang, additional, Ekkernkamp, Axel, additional, Rehahn, Kerstin, additional, Martus, Peter, additional, Volk, Hans-Dieter, additional, Unterwalder, Nadine, additional, Kölsch, Uwe, additional, Brommer, Benedikt, additional, Hellmann, Rick C, additional, Baumgartner, Elias, additional, Hirt, Julian, additional, Geurtz, Laura-Christin, additional, Saidy, Ramin Raul Ossami, additional, Prüss, Harald, additional, Laginha, Ines, additional, Failli, Vieri, additional, Grittner, Ulrike, additional, Dirnagl, Ulrich, additional, and Schwab, Jan M, additional

Published
2023
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8. The spinal cord injury-induced immune deficiency syndrome: results of the SCIentinel study

Author

Kopp, Marcel A, Meisel, Christian, Liebscher, Thomas, Watzlawick, Ralf, Cinelli, Paolo, Schweizerhof, Oliver, Blex, Christian, Lübstorf, Tom, Prilipp, Erik, Niedeggen, Andreas, Druschel, Claudia, Schaser, Klaus-Dieter, Wanner, Guido A, Curt, Armin, Lindemann, Gertraut, Nugeva, Natalia, Fehlings, Michael G, Vajkoczy, Peter, Cabraja, Mario, Dengler, Julius, Ertel, Wolfgang, Ekkernkamp, Axel, Rehahn, Kerstin, Martus, Peter, Volk, Hans-Dieter, Unterwalder, Nadine, Kölsch, Uwe, Brommer, Benedikt, Hellmann, Rick C, Baumgartner, Elias, et al, and University of Zurich

Subjects
10021 Department of Trauma Surgery, 610 Medicine & health
Published
2023

9. The spinal cord injury-induced immune deficiency syndrome: results of the SCIentinel study

Author

Kopp, Marcel A; https://orcid.org/0000-0001-6832-9599, Meisel, Christian; https://orcid.org/0000-0003-0222-991X, Liebscher, Thomas; https://orcid.org/0000-0002-6025-6564, Watzlawick, Ralf, Cinelli, Paolo; https://orcid.org/0000-0002-0163-9055, Schweizerhof, Oliver, Blex, Christian, Lübstorf, Tom, Prilipp, Erik, Niedeggen, Andreas, Druschel, Claudia, Schaser, Klaus-Dieter, Wanner, Guido A, Curt, Armin, Lindemann, Gertraut, Nugeva, Natalia, Fehlings, Michael G; https://orcid.org/0000-0002-5722-6364, Vajkoczy, Peter, Cabraja, Mario, Dengler, Julius, Ertel, Wolfgang, Ekkernkamp, Axel, Rehahn, Kerstin, Martus, Peter, Volk, Hans-Dieter, Unterwalder, Nadine, Kölsch, Uwe, Brommer, Benedikt, Hellmann, Rick C, Baumgartner, Elias, et al, Kopp, Marcel A; https://orcid.org/0000-0001-6832-9599, Meisel, Christian; https://orcid.org/0000-0003-0222-991X, Liebscher, Thomas; https://orcid.org/0000-0002-6025-6564, Watzlawick, Ralf, Cinelli, Paolo; https://orcid.org/0000-0002-0163-9055, Schweizerhof, Oliver, Blex, Christian, Lübstorf, Tom, Prilipp, Erik, Niedeggen, Andreas, Druschel, Claudia, Schaser, Klaus-Dieter, Wanner, Guido A, Curt, Armin, Lindemann, Gertraut, Nugeva, Natalia, Fehlings, Michael G; https://orcid.org/0000-0002-5722-6364, Vajkoczy, Peter, Cabraja, Mario, Dengler, Julius, Ertel, Wolfgang, Ekkernkamp, Axel, Rehahn, Kerstin, Martus, Peter, Volk, Hans-Dieter, Unterwalder, Nadine, Kölsch, Uwe, Brommer, Benedikt, Hellmann, Rick C, Baumgartner, Elias, and et al

Abstract

Infections are prevalent after spinal cord injury (SCI), constitute the main cause of death and are a rehabilitation confounder associated with impaired recovery. We hypothesize that SCI causes an acquired lesion-dependent (neurogenic) immune suppression as an underlying mechanism to facilitate infections. The international prospective multicentre cohort study (SCIentinel; protocol registration DRKS00000122; n = 111 patients) was designed to distinguish neurogenic from general trauma-related effects on the immune system. Therefore, SCI patient groups differing by neurological level, i.e. high SCI [thoracic (Th)4 or higher]; low SCI (Th5 or lower) and severity (complete SCI; incomplete SCI), were compared with a reference group of vertebral fracture (VF) patients without SCI. The primary outcome was quantitative monocytic Human Leukocyte Antigen-DR expression (mHLA-DR, synonym MHC II), a validated marker for immune suppression in critically ill patients associated with infection susceptibility. mHLA-DR was assessed from Day 1 to 10 weeks after injury by applying standardized flow cytometry procedures. Secondary outcomes were leucocyte subpopulation counts, serum immunoglobulin levels and clinically defined infections. Linear mixed models with multiple imputation were applied to evaluate group differences of logarithmic-transformed parameters. Mean quantitative mHLA-DR [ln (antibodies/cell)] levels at the primary end point 84 h after injury indicated an immune suppressive state below the normative values of 9.62 in all groups, which further differed in its dimension by neurological level: high SCI [8.95 (98.3% confidence interval, CI: 8.63; 9.26), n = 41], low SCI [9.05 (98.3% CI: 8.73; 9.36), n = 29], and VF without SCI [9.25 (98.3% CI: 8.97; 9.53), n = 41, P = 0.003]. Post hoc analysis accounting for SCI severity revealed the strongest mHLA-DR decrease [8.79 (95% CI: 8.50; 9.08)] in the complete, high SCI group, further demonstrating delayed mHLA-DR recovery [9.08 (

Published
2023

10. IRAK1 Duplication in MECP2 Duplication Syndrome Does Not Increase Canonical NF-κB–Induced Inflammation

Author

Gottschalk, Ilona, primary, Kölsch, Uwe, additional, Wagner, Dimitrios L., additional, Kath, Jonas, additional, Martini, Stefania, additional, Krüger, Renate, additional, Puel, Anne, additional, Casanova, Jean-Laurent, additional, Jezela-Stanek, Aleksandra, additional, Rossi, Rainer, additional, Chehadeh, Salima El, additional, Van Esch, Hilde, additional, and von Bernuth, Horst, additional

Published
2022
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11. A rare case of HLA-B27 negative sacroiliitis in a patient with genetically impaired immunomodulatory function of regulatory T cells

Author

Bossaller, Lukas, Freiin von Rheinbaben, Sabrina, Kölsch, Uwe, Von Osten, Heimke, Ribback, Silvia, Fischer, Annika, Langner, Sönke, Ehlert, Karoline, Lode, Holger N, Grimbacher, Bodo, and Meyer-Bahlburg, Almut

Subjects
Medicine and health
Abstract

History: An 18-year-old male with a history of genetically and functionally proven CTLA-4 insufficiency complained about inflammatory back pain. His past medical history was significant for autoimmune hemolytic anemia, which lead to splenectomy at age 6, followed by pneumococcal meningitis and overwhelming [for full text, please go to the a.m. URL]

Published
2022
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12. Im Routinelabor angekommen.

Author

Sack, Ulrich and Kölsch, Uwe

Subjects
*IMMUNE system, *ANTIGENS, *PATHOGENIC microorganisms, *IMMUNE response, *VACCINE effectiveness
Abstract

The article presents the discussion on human immune system possessing two fundamental recognition mechanisms as part of acquired immunity to initiate antigen-specific responses against pathogens. Topics include providing insights into previous exposure to specific pathogens and the development of immune responses; and offering insights into existing protective immunity or vaccine efficacy assessment.

Published
2023
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14. Non-Skewed X-inactivation Results in NF-κB Essential Modulator (NEMO) Δ-exon 5-autoinflammatory Syndrome (NEMO-NDAS) in a Female with Incontinentia Pigmenti.

Author

Eigemann J, Janda A, Schuetz C, Lee-Kirsch MA, Schulz A, Hoenig M, Furlan I, Jacobsen EM, Zinngrebe J, Peters S, Drewes C, Siebert R, Rump EM, Führer M, Lorenz M, Pannicke U, Kölsch U, Debatin KM, von Bernuth H, Schwarz K, and Felgentreff K

Subjects
Humans, Female, Hereditary Autoinflammatory Diseases genetics, Hereditary Autoinflammatory Diseases diagnosis, Mutation genetics, Cytokines metabolism, Adult, Alternative Splicing, Signal Transduction, Incontinentia Pigmenti genetics, Incontinentia Pigmenti diagnosis, I-kappa B Kinase genetics, X Chromosome Inactivation, Exons genetics
Abstract

Purpose: Genetic hypomorphic defects in X chromosomal IKBKG coding for the NF-κB essential modulator (NEMO) lead to ectodermal dysplasia and immunodeficiency in males and the skin disorder incontinentia pigmenti (IP) in females, respectively. NF-κB essential modulator (NEMO) Δ-exon 5-autoinflammatory syndrome (NEMO-NDAS) is a systemic autoinflammatory disease caused by alternative splicing and increased proportion of NEMO-Δex5. We investigated a female carrier presenting with IP and NEMO-NDAS due to non-skewed X-inactivation., Methods: IKBKG transcripts were quantified in peripheral blood mononuclear cells isolated from the patient, her mother, and healthy controls using RT-PCR and nanopore sequencing. Corresponding proteins were analyzed by western blotting and flow cytometry. Besides toll-like receptor (TLR) and tumor necrosis factor (TNF) signaling, the interferon signature, cytokine production and X-inactivation status were investigated., Results: IP and autoinflammation with recurrent fever, oral ulcers, hepatitis, and neutropenia, but no immunodeficiency was observed in a female patient. Besides moderately reduced NEMO signaling function, type I interferonopathy, and elevated IL-18 and CXCL10 were found. She and her mother both carried the heterozygous variant c.613 C > T p.(Gln205*) in exon 5 of IKBKG previously reported in NEMO-deficient patients. However, X-inactivation was skewed in the mother, but not in the patient. Alternative splicing led to increased ratios of NEMO-Dex5 over full-length protein in peripheral blood cell subsets causing autoinflammation. Clinical symptoms partially resolved under treatment with TNF inhibitors., Conclusion: Non-skewed X-inactivation can lead to NEMO-NDAS in females with IP carrying hypomorphic IKBKG variants due to alternative splicing and increased proportions of NEMO-∆ex5., (© 2024. The Author(s).)

Published
2024
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