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15 results on '"Sic, Heiko"'

1. Sphingosine-1-phosphate receptors control B-cell migration through signaling components associated with primary immunodeficiencies, chronic lymphocytic leukemia, and multiple sclerosis

Author

Sic, Heiko, Kraus, Helene, Madl, Josef, Flittner, Karl-Andreas, von Münchow, Audrey Lilly, Pieper, Kathrin, Rizzi, Marta, Kienzler, Anne-Kathrin, Ayata, Korcan, Rauer, Sebastian, Kleuser, Burkhard, Salzer, Ulrich, Burger, Meike, Zirlik, Katja, Lougaris, Vassilios, Plebani, Alessandro, Römer, Winfried, Loeffler, Christoph, Scaramuzza, Samantha, Villa, Anna, Noguchi, Emiko, Grimbacher, Bodo, and Eibel, Hermann

Published
2014
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5. A common single nucleotide polymorphism impairs B-cell activating factor receptorʼs multimerization, contributing to common variable immunodeficiency

Author

Pieper, Kathrin, Rizzi, Marta, Speletas, Matthaios, Smulski, Cristian R., Sic, Heiko, Kraus, Helene, Salzer, Ulrich, Fiala, Gina J., Schamel, Wolfgang W., Lougaris, Vassilios, Plebani, Alessandro, Hammarstrom, Lennart, Recher, Mike, Germenis, Anastasios E., Grimbacher, Bodo, Warnatz, Klaus, Rolink, Antonius G., Schneider, Pascal, Notarangelo, Luigi D., and Eibel, Hermann

Published
2014
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6. An Activating Janus Kinase-3 Mutation Is Associated with Cytotoxic T Lymphocyte Antigen-4-Dependent Immune Dysregulation Syndrome

Author

Sic, Heiko, primary, Speletas, Matthaios, additional, Cornacchione, Vanessa, additional, Seidl, Maximillian, additional, Beibel, Martin, additional, Linghu, Bolan, additional, Yang, Fan, additional, Sevdali, Eirini, additional, Germenis, Anastasios E., additional, Oakeley, Edward J., additional, Vangrevelinghe, Eric, additional, Sailer, Andreas W., additional, Traggiai, Elisabetta, additional, Gram, Hermann, additional, and Eibel, Hermann, additional

Published
2017
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7. Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity

Author

Willmann, Katharina L., Klaver, Stefanie, Doğu, Figen, Santos-Valente, Elisangela, Garncarz, Wojciech, Bilic, Ivan, Mace, Emily, Salzer, Elisabeth, Domínguez Conde, Cecilia, Sic, Heiko, Májek, Peter, Banerjee, Pinaki P., Vladimer, Gregory I., Haskoloğlu, Şule, Gökalp Bolkent, Musa, Küpesiz, Alphan, Condino-Neto, Antonio, Colinge, Jacques, Superti-Furga, Giulio, Pickl, Winfried F., van Zelm, Menno C., Eibel, Hermann, Orange, Jordan S., Ikincioğulları, Aydan, Boztuğ, Kaan, Immunology, Institut de recherche en cancérologie de Montpellier (IRCM - U896 Inserm - UM1), and Université Montpellier 1 (UM1)-CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)

Subjects
Protein-Serine-Threonine Kinases/*genetics, T-Lymphocytes, Cryptosporidiosis, [SDV.CAN]Life Sciences [q-bio]/Cancer, Protein Serine-Threonine Kinases, Article, Inducible T-Cell Co-Stimulator Ligand, Leukocyte Count, Agammaglobulinemia, Recurrence, Lymphopenia, Virus Diseases/immunology, Humans, Cryptosporidiosis/immunology, Killer Cells, Computer Simulation, Inducible T-Cell Co-Stimulator Ligand/metabolism, Lymphocyte Count, Child, Preschool, B-Lymphocytes, Helper-Inducer/immunology, Immunologic Deficiency Syndromes, Infant, B-Lymphocytes/immunology, Bacterial Infections, T-Lymphocytes, Helper-Inducer, Immunoglobulin Class Switching, Pedigree, Killer Cells, Natural, Bacterial Infections/immunology, Natural/immunology, Virus Diseases, Child, Preschool, Mutation, Female, Immunologic Deficiency Syndromes/genetics, Lymphopenia/*genetics/immunology, Immunologic Memory, Agammaglobulinemia/*genetics/immunology
Abstract

Primary immunodeficiency disorders enable identification of genes with crucial roles in the human immune system. Here we study patients suffering from recurrent bacterial, viral and Cryptosporidium infections, and identify a biallelic mutation in the MAP3K14 gene encoding NIK (NF-κB-inducing kinase). Loss of kinase activity of mutant NIK, predicted by in silico analysis and confirmed by functional assays, leads to defective activation of both canonical and non-canonical NF-κB signalling. Patients with mutated NIK exhibit B-cell lymphopenia, decreased frequencies of class-switched memory B cells and hypogammaglobulinemia due to impaired B-cell survival, and impaired ICOSL expression. Although overall T-cell numbers are normal, both follicular helper and memory T cells are perturbed. Natural killer (NK) cells are decreased and exhibit defective activation, leading to impaired formation of NK-cell immunological synapses. Collectively, our data illustrate the non-redundant role for NIK in human immune responses, demonstrating that loss-of-function mutations in NIK can cause multiple aberrations of lymphoid immunity., Primary immunodeficiency disorders can be used to identify key immune functions. Here, the authors identify a biallelic mutation in the gene encoding NF-κB-inducing kinase in a family suffering a range of infections, and show that it causes defects in NK and T-cell function and has broad effects on B-cell function.

Published
2014

8. Deficiency of the B Cell-Activating Factor Receptor Results in Limited CD169 + Macrophage Function during Viral Infection

Author

Xu, Haifeng C., primary, Huang, Jun, additional, Khairnar, Vishal, additional, Duhan, Vikas, additional, Pandyra, Aleksandra A., additional, Grusdat, Melanie, additional, Shinde, Prashant, additional, McIlwain, David R., additional, Maney, Sathish Kumar, additional, Gommerman, Jennifer, additional, Löhning, Max, additional, Ohashi, Pamela S., additional, Mak, Tak W., additional, Pieper, Kathrin, additional, Sic, Heiko, additional, Speletas, Matthaios, additional, Eibel, Hermann, additional, Ware, Carl F., additional, Tumanov, Alexei V., additional, Kruglov, Andrey A., additional, Nedospasov, Sergei A., additional, Häussinger, Dieter, additional, Recher, Mike, additional, Lang, Karl S., additional, and Lang, Philipp A., additional

Published
2015
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9. IL-10 Critically Modulates B Cell Responsiveness in Rankl−/− Mice

Author

Marrella, Veronica, primary, Lo Iacono, Nadia, additional, Fontana, Elena, additional, Sobacchi, Cristina, additional, Sic, Heiko, additional, Schena, Francesca, additional, Sereni, Lucia, additional, Castiello, Maria Carmina, additional, Poliani, Pietro Luigi, additional, Vezzoni, Paolo, additional, Cassani, Barbara, additional, Traggiai, Elisabetta, additional, and Villa, Anna, additional

Published
2015
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10. Deficiency of MALT1 Paracaspase Activity Results in Unbalanced Regulatory and Effector T and B Cell Responses Leading to Multiorgan Inflammation

Author

Bornancin, Frédéric, primary, Renner, Florian, additional, Touil, Ratiba, additional, Sic, Heiko, additional, Kolb, Yeter, additional, Touil-Allaoui, Ismahane, additional, Rush, James S., additional, Smith, Paul A., additional, Bigaud, Marc, additional, Junker-Walker, Ursula, additional, Burkhart, Christoph, additional, Dawson, Janet, additional, Niwa, Satoru, additional, Katopodis, Andreas, additional, Nuesslein-Hildesheim, Barbara, additional, Weckbecker, Gisbert, additional, Zenke, Gerhard, additional, Kinzel, Bernd, additional, Traggiai, Elisabetta, additional, Brenner, Dirk, additional, Brüstle, Anne, additional, St. Paul, Michael, additional, Zamurovic, Natasa, additional, McCoy, Kathy D., additional, Rolink, Antonius, additional, Régnier, Catherine H., additional, Mak, Tak W., additional, Ohashi, Pamela S., additional, Patel, Dhavalkumar D., additional, and Calzascia, Thomas, additional

Published
2015
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11. High Levels of SOX5 Decrease Proliferative Capacity of Human B Cells, but Permit Plasmablast Differentiation

Author

Rakhmanov, Mirzokhid, primary, Sic, Heiko, additional, Kienzler, Anne-Kathrin, additional, Fischer, Beate, additional, Rizzi, Marta, additional, Seidl, Maximilian, additional, Melkaoui, Kerstina, additional, Unger, Susanne, additional, Moehle, Luisa, additional, Schmit, Nadine E., additional, Deshmukh, Sachin D., additional, Ayata, Cemil Korcan, additional, Schuh, Wolfgang, additional, Zhang, Zhibing, additional, Cosset, François-Loic, additional, Verhoeyen, Els, additional, Peter, Hans-Hartmut, additional, Voll, Reinhard E., additional, Salzer, Ulrich, additional, Eibel, Hermann, additional, and Warnatz, Klaus, additional

Published
2014
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12. A Feeder-Free Differentiation System Identifies Autonomously Proliferating B Cell Precursors in Human Bone Marrow

Author

Kraus, Helene, primary, Kaiser, Sandra, additional, Aumann, Konrad, additional, Bönelt, Peter, additional, Salzer, Ulrich, additional, Vestweber, Dietmar, additional, Erlacher, Miriam, additional, Kunze, Mirjam, additional, Burger, Meike, additional, Pieper, Kathrin, additional, Sic, Heiko, additional, Rolink, Antonius, additional, Eibel, Hermann, additional, and Rizzi, Marta, additional

Published
2014
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13. B cell homeostasis is disturbed by immunosuppressive therapies in patients with ANCA-associated vasculitides

Author

Thiel, Jens, primary, Salzer, Ulrich, additional, Hässler, Fabian, additional, Effelsberg, Nora M., additional, Hentze, Carolin, additional, Sic, Heiko, additional, Bartsch, Marit, additional, Miehle, Nikolaus, additional, Peter, Hans Hartmut, additional, Warnatz, Klaus, additional, Schlesier, Michael, additional, Voll, Reinhard E., additional, and Venhoff, Nils, additional

Published
2013
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14. Deficiency of the B cell-activating factor receptor results in limited CD169+ macrophage function during viral infection.

Author

Xu HC, Huang J, Khairnar V, Duhan V, Pandyra AA, Grusdat M, Shinde P, McIlwain DR, Maney SK, Gommerman J, Löhning M, Ohashi PS, Mak TW, Pieper K, Sic H, Speletas M, Eibel H, Ware CF, Tumanov AV, Kruglov AA, Nedospasov SA, Häussinger D, Recher M, Lang KS, and Lang PA

Subjects
Adaptive Immunity, Animals, Immunity, Innate, Interferon Type I metabolism, Lymphocytic choriomeningitis virus immunology, Mice, Knockout, Signal Transduction, Vesiculovirus immunology, Arenaviridae Infections immunology, Macrophages chemistry, Macrophages immunology, Receptors, Interleukin-4 deficiency, Rhabdoviridae Infections immunology, Sialic Acid Binding Ig-like Lectin 1 analysis
Abstract

Unlabelled: The B cell-activating factor (BAFF) is critical for B cell development and humoral immunity in mice and humans. While the role of BAFF in B cells has been widely described, its role in innate immunity remains unknown. Using BAFF receptor (BAFFR)-deficient mice, we characterized BAFFR-related innate and adaptive immune functions following infection with vesicular stomatitis virus (VSV) and lymphocytic choriomeningitis virus (LCMV). We identified a critical role for BAFFR signaling in the generation and maintenance of the CD169(+) macrophage compartment. Consequently, Baffr(-) (/) (-) mice exhibited limited induction of innate type I interferon production after viral infection. Lack of BAFFR signaling reduced virus amplification and presentation following viral infection, resulting in highly reduced antiviral adaptive immune responses. As a consequence, BAFFR-deficient mice showed exacerbated and fatal disease after viral infection. Mechanistically, transient lack of B cells in Baffr(-) (/) (-) animals resulted in limited lymphotoxin expression, which is critical for maintenance of CD169(+) cells. In conclusion, BAFFR signaling affects both innate and adaptive immune activation during viral infections., Importance: Viruses cause acute and chronic infections in humans resulting in millions of deaths every year. Innate immunity is critical for the outcome of a viral infection. Innate type I interferon production can limit viral replication, while adaptive immune priming by innate immune cells induces pathogen-specific immunity with long-term protection. Here, we show that BAFFR deficiency not only perturbed B cells, but also resulted in limited CD169(+) macrophages. These macrophages are critical in amplifying viral particles to trigger type I interferon production and initiate adaptive immune priming. Consequently, BAFFR deficiency resulted in reduced enforced viral replication, limited type I interferon production, and reduced adaptive immunity compared to BAFFR-competent controls. As a result, BAFFR-deficient mice were predisposed to fatal viral infections. Thus, BAFFR expression is critical for innate immune activation and antiviral immunity., (Copyright © 2015, American Society for Microbiology. All Rights Reserved.)

Published
2015
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15. Biallelic loss-of-function mutation in NIK causes a primary immunodeficiency with multifaceted aberrant lymphoid immunity.

Author

Willmann KL, Klaver S, Doğu F, Santos-Valente E, Garncarz W, Bilic I, Mace E, Salzer E, Conde CD, Sic H, Májek P, Banerjee PP, Vladimer GI, Haskoloğlu S, Bolkent MG, Küpesiz A, Condino-Neto A, Colinge J, Superti-Furga G, Pickl WF, van Zelm MC, Eibel H, Orange JS, Ikincioğulları A, and Boztuğ K

Subjects
Agammaglobulinemia immunology, B-Lymphocytes immunology, Bacterial Infections immunology, Child, Preschool, Computer Simulation, Cryptosporidiosis immunology, Female, Humans, Immunoglobulin Class Switching, Immunologic Deficiency Syndromes genetics, Immunologic Memory, Inducible T-Cell Co-Stimulator Ligand metabolism, Infant, Killer Cells, Natural immunology, Leukocyte Count, Lymphocyte Count, Lymphopenia immunology, Mutation, Pedigree, Recurrence, T-Lymphocytes, Helper-Inducer immunology, Virus Diseases immunology, NF-kappaB-Inducing Kinase, Agammaglobulinemia genetics, Lymphopenia genetics, Protein Serine-Threonine Kinases genetics
Abstract

Primary immunodeficiency disorders enable identification of genes with crucial roles in the human immune system. Here we study patients suffering from recurrent bacterial, viral and Cryptosporidium infections, and identify a biallelic mutation in the MAP3K14 gene encoding NIK (NF-κB-inducing kinase). Loss of kinase activity of mutant NIK, predicted by in silico analysis and confirmed by functional assays, leads to defective activation of both canonical and non-canonical NF-κB signalling. Patients with mutated NIK exhibit B-cell lymphopenia, decreased frequencies of class-switched memory B cells and hypogammaglobulinemia due to impaired B-cell survival, and impaired ICOSL expression. Although overall T-cell numbers are normal, both follicular helper and memory T cells are perturbed. Natural killer (NK) cells are decreased and exhibit defective activation, leading to impaired formation of NK-cell immunological synapses. Collectively, our data illustrate the non-redundant role for NIK in human immune responses, demonstrating that loss-of-function mutations in NIK can cause multiple aberrations of lymphoid immunity.

Published
2014
Full Text
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