Browsing by Author "Espanol, Teresa"

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    Mutations in the signal transducer and activator of transcription 3 (STAT3) and diagnostic guidelines for the Hyper-IgE Syndrome
    (Wiley, 2010-04) Woellner, Cristina; Gertz, M. E.; Schaffer, Alejandro; Lagos, Macarena; Perro, Mario; Glocker, Erik-Oliver; Pietrogrande, Maria Cristina; Cossu, Fausto; Marin Franco, Jose Luis; Matamoros, N.; Pietrucha, Bernard; Heropolitanska-Pliszka, Edyta; Yeganch, M.; Rezaei, Nima; Espanol, Teresa; Ehl, Stephan; Gennery, Andrew R.; Abinun, Mario; Breborowicz, Anna; Niehues, Tim; Junker, Anne K.; Turvey, Stuart E.; Plebani, Alessandro; Sanchez, Berta Erika Luis; Garty, Ben Zion; Pignata, Claudio; Cancrini, Caterina; Litzman, Jiří; Sanal, Özden; Batimann, U.; Bacchetta, Rosa; Hsu, Amy P.; Davis, Joie N.; Hammarström, Lennart L.G.; Davis, Edward Graham; Eren, Efrem; Arkwright, Peter D.; Moilanen, Jukka S.; Viemann, Dorothee; Khan, Sujoy; Máródi, László D.R.; Cant, Andrew James; Freeman, Alexandra F.; Puck, Jennifer M.; Holland, Steven M.; Grimbacher, Bodo; Kılıç, Sara Şebnem; Uludağ Üniversitesi/Tıp Fakültesi/Çocuk Sağlığı ve Hastalıkları Anabilim Dalı.; AAH-1658-2021
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    Toll-like receptor stimulation induces higher tnf-α secretion in peripheral blood mononuclear cells from patients with hyper ige syndrome
    (Karger, 2008-01-01) Yeganeh, Mehdi; Henneke, Philipp; Rezaei, Nima; Ehl, Stephan; Thiel, Doerte; Matamoros, Nuria; Pietrogrande, Cristina; Espanol, Teresa; Litzman, Jiri; Franco, Jose L.; Sanal, Ozden; Kılıç, Sara S.; Breborowicz, Anna; Plebani, Alessandro; Renner, Ellen; Rothenfusser, Simon; Hawn, Thomas R.; Woellner, Cristina; Grimbacher, Bodo; KILIÇ GÜLTEKİN, SARA ŞEBNEM; Uludağ Üniversitesi/Tıp Fakültesi/Pediatrik İmmünoloji Anabilim Dalı.; 0000-0002-9454-1603; 0000-0002-1926-5426; 0000-0001-8571-2581; 0000-0002-5398-1717; 0000-0001-9816-8538; 0000-0002-6897-6806; AAH-1658-2021
    Hyper IgE syndromes (HIES) are primary immunodeficiency disorders of unknown pathogenesis. Patients are typically affected with 'cold' abscesses of the skin, recurrent cyst-forming pneumonia, chronic mucocutaneous candidiasis and other less frequent features such as progressive skeletal abnormalities. Defective signaling in the Toll-like receptor (TLR) pathways has been suggested as a responsible pathologic mechanism, however, in previous reports, 10 patients revealed no defect in inflammatory cytokine responses to different TLR ligands. Here, we report the increase in pro-inflammatory cytokines TNF-alpha and IL-8, following TLR2 and TLR4 stimulation in a larger cohort of 25 additional patients with HIES, and provide a meta-analysis of the TLR data in HIES. Copyright (C) 2008 S. Karger AG, Basel.