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52. Neutralizing antibody responses 300 days after SARS‐CoV‐2 infection and induction of high antibody titers after vaccination

Author

Urlaub, Doris, primary, Wolfsdorff, Natalie, additional, Hoffmann, Jan‐Erik, additional, Dorok, Stefanie, additional, Hoffmann, Markus, additional, Anft, Moritz, additional, Pieris, Naomi, additional, Günther, Patrick, additional, Schaaf, Bernhard, additional, Cassens, Uwe, additional, Bröde, Peter, additional, Claus, Maren, additional, Picard, Lea K., additional, Wingert, Sabine, additional, Backes, Simone, additional, Durak, Deniz, additional, Babel, Nina, additional, Pöhlmann, Stefan, additional, Renken, Frank, additional, Raunser, Stefan, additional, and Watzl, Carsten, additional

Published
2022
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53. Impact of Biological and Lifestyle Factors on Cognitive Aging and Work Ability in the Dortmund Vital Study: Protocol of an Interdisciplinary, Cross-sectional, and Longitudinal Study

Author

Gajewski, Patrick D, primary, Getzmann, Stephan, additional, Bröde, Peter, additional, Burke, Michael, additional, Cadenas, Cristina, additional, Capellino, Silvia, additional, Claus, Maren, additional, Genç, Erhan, additional, Golka, Klaus, additional, Hengstler, Jan G, additional, Kleinsorge, Thomas, additional, Marchan, Rosemarie, additional, Nitsche, Michael A, additional, Reinders, Jörg, additional, van Thriel, Christoph, additional, Watzl, Carsten, additional, and Wascher, Edmund, additional

Published
2022
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55. Inhibition of Glucose Uptake Blocks Proliferation but Not Cytotoxic Activity of NK Cells

Author

Picard, Lea Katharina, Littwitz-Salomon, Elisabeth, Waldmann, Herbert, and Watzl, Carsten

Subjects
Medizin, natural killer cells, metabolism, cytokines, glucose transporter, degranulation
Abstract

Tumor cells often have very high energy demands. Inhibition of glucose uptake is therefore a possible approach to limit the proliferation and survival of transformed cells. However, immune cells also require energy to initiate and to maintain anti-tumor immune reactions. Here, we investigate the effect of Glutor, an inhibitor of glucose transporters, on the function of human Natural Killer (NK) cells, which are important for the immunosurveillance of cancer. Glutor treatment effectively inhibits glycolysis in NK cells. However, acute treatment with the inhibitor has no effect on NK cell effector functions. Prolonged inhibition of glucose uptake by Glutor prevents the proliferation of NK cells, increases their pro-inflammatory regulatory function and reduces the stimulation-dependent production of IFN-γ. Interestingly, even after prolonged Glutor treatment NK cell cytotoxicity and serial killing activity were still intact, demonstrating that cytotoxic NK cell effector functions are remarkably robust against metabolic disturbances. CA extern

Published
2022

57. Effect of JAK Inhibition on the Induction of Proinflammatory HLA – DR + CD90 + Rheumatoid Arthritis Synovial Fibroblasts by Interferon‐γ

Author

Zhao, Shuyang, primary, Grieshaber‐Bouyer, Ricardo, additional, Rao, Deepak A., additional, Kolb, Philipp, additional, Chen, Haizhang, additional, Andreeva, Ivana, additional, Tretter, Theresa, additional, Lorenz, Hanns‐Martin, additional, Watzl, Carsten, additional, Wabnitz, Guido, additional, Tykocinski, Lars‐Oliver, additional, and Merkt, Wolfgang, additional

Published
2022
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58. Impact of Biological and Lifestyle Factors on Cognitive Aging and Work Ability in the Dortmund Vital Study: Protocol of an Interdisciplinary, Cross-sectional, and Longitudinal Study (Preprint)

Author

Gajewski, Patrick D, primary, Getzmann, Stephan, additional, Bröde, Peter, additional, Burke, Michael, additional, Cadenas, Cristina, additional, Capellino, Silvia, additional, Claus, Maren, additional, Genç, Erhan, additional, Golka, Klaus, additional, Hengstler, Jan G, additional, Kleinsorge, Thomas, additional, Marchan, Rosemarie, additional, Nitsche, Michael A, additional, Reinders, Jörg, additional, van Thriel, Christoph, additional, Watzl, Carsten, additional, and Wascher, Edmund, additional

Published
2021
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59. Spatio-Temporal Multiscale Analysis of Western Diet-Fed Mice Reveals a Translationally Relevant Sequence of Events during NAFLD Progression

Author

Ghallab, Ahmed, primary, Myllys, Maiju, additional, Friebel, Adrian, additional, Duda, Julia, additional, Edlund, Karolina, additional, Halilbasic, Emina, additional, Vucur, Mihael, additional, Hobloss, Zaynab, additional, Brackhagen, Lisa, additional, Begher-Tibbe, Brigitte, additional, Hassan, Reham, additional, Burke, Michael, additional, Genc, Erhan, additional, Frohwein, Lynn Johann, additional, Hofmann, Ute, additional, Holland, Christian H., additional, González, Daniela, additional, Keller, Magdalena, additional, Seddek, Abdel-latif, additional, Abbas, Tahany, additional, Mohammed, Elsayed S. I., additional, Teufel, Andreas, additional, Itzel, Timo, additional, Metzler, Sarah, additional, Marchan, Rosemarie, additional, Cadenas, Cristina, additional, Watzl, Carsten, additional, Nitsche, Michael A., additional, Kappenberg, Franziska, additional, Luedde, Tom, additional, Longerich, Thomas, additional, Rahnenführer, Jörg, additional, Hoehme, Stefan, additional, Trauner, Michael, additional, and Hengstler, Jan G., additional

Published
2021
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61. Humoral and cellular immune responses to repeated SARS‐CoV‐2 infection and vaccination in an individual living with HIV.

Author

Simsek, Agit, Bessen, Clara, Meister, Toni L, Urlaub, Doris, Skaletz‐Rorowski, Adriane, Brockmeyer, Norbert H, Overheu, Oliver, Reinacher‐Schick, Anke, Faissner, Simon, Watzl, Carsten, Pfaender, Stephanie, Schmitz, Ingo, Potthoff, Anja, and Plaza‐Sirvent, Carlos

Subjects
SARS-CoV-2, VACCINATION, REGULATORY T cells, SARS-CoV-2 Delta variant, HIV
Abstract

Similarly, while patient's plasma was not able to neutralize SARS-CoV-2 in vitro following first infection, the WT variant was strongly neutralized after the first vaccination. Humoral and cellular immune responses to repeated SARS-CoV-2 infection and vaccination in an individual living with HIV T cells targeting SARS-CoV-2: by infection, vaccination, and against future variants. [Extracted from the article]

Published
2023
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62. Low self-reported stress despite immune-physiological changes in paramedics during rescue operations

Author

Peifer, Corinna, Hagemann, Vera, Claus, Maren, Larra, Mauro F., Aust, Fabienne, Kühn, Marvin, Owczarek, Monika, Bröde, Peter, Pacharra, Marlene, Steffens, Holger, Watzl, Carsten, Wascher, Edmund, and Capellino, Silvia

Subjects
coping, work/psychological demands, heart rate variability, cortisol, burnout, immune system, stress, 0303 health sciences, 03 medical and health sciences, 030311 toxicology, Original Article
Abstract

Despite the high stress levels, paramedics seem to ignore or even negate the stress. This can be detrimental and lead to stress-related diseases. Therefore, we investigated the divergence between physiological and psychological stress responses of paramedics. Participants were 16 paramedics and 17 white-collar workers. We assessed psychological stress parameters, cortisol awakening response (CAR), and quantified immune parameters. In paramedics, electrocardiogram (ECG) was measured during one complete 24-hour shift. Our results revealed that CAR was higher in paramedics compared to controls. An alteration of immune parameters was observed even during days of free time. Also, ECG recordings showed acute stress in paramedics during rescue situations. Questionnaires revealed that rescue-service specific stressors affect psychological outcomes. However, paramedics reported significantly less mental stress and higher levels of depersonalization than controls. Taken together, our results suggest higher stress in paramedics compared to controls. However, paramedics negate their daily stress. Our findings underline therefore the importance to develop stress-management interventions for paramedics including sensitization for their stress reactions., EXCLI Journal; 20:Doc792; ISSN 1611-2156

Published
2021

63. Impact of N6-methyladenosine (m6A) modification on immunity.

Author

Elsabbagh, Raghda A., Rady, Mona, Watzl, Carsten, Abou-Aisha, Khaled, and Gad, Mohamed Z.

Subjects
ADENOSINES, IMMUNITY, LINCRNA, IMMUNE system, IMMUNE response, CELL physiology
Abstract

N6-methyl-adenosine (m6A) is the most prevalent modification on mRNAs and long noncoding RNAs (lnRNAs) in higher eukaryotes. Modulation of m6A relies on m6A writers, erasers and readers. m6A modification contributes to diverse fundamental biological functions at the molecular, cellular, and physiological levels. The dysregulation of m6A modification has been implicated in various human diseases. Thus, m6A modification has now become a research hotspot for its potential therapeutic applications in the treatment of various cancers and diseases. The immune system is essential to provide defense against infections and cancers. This review summarizes the current knowledge about the roles of m6A in regulating immune cell functions and immune responses. 86-zz-Q3pVueCk-bZrqu3a Video abstract [ABSTRACT FROM AUTHOR]

Published
2022
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65. Activating Natural Killer Cell Receptors, Selectins, and Inhibitory Siglecs Recognize Ebolavirus Glycoprotein

Author

Jarahian, Mostafa, primary, Marstaller, Katharina, additional, Banna, Nadine, additional, Ahani, Roshanak, additional, Etemadzadeh, Mohammad Hossein, additional, Boller, Lea K., additional, Azadmanesh, Kayhan, additional, Cid-Arregui, Angel, additional, Khezri, Abdolrahman, additional, Berger, Martin R., additional, Momburg, Frank, additional, and Watzl, Carsten, additional

Published
2021
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67. Effect of JAK Inhibition on the Induction of Proinflammatory HLA–DR+CD90+ Rheumatoid Arthritis Synovial Fibroblasts by Interferon-γ

Author

Zhao, Shuyang, Grieshaber-Bouyer, Dr. Ricardo, Rao, Deepak, Kolb, Philipp, Chen, Haizhang, Andreeva, Ivana, Tretter, Theresa, Lorenz, Hanns-Martin, Watzl, Carsten, Wabnitz, Guido, Tykocinski, Lars-Oliver, and Merkt, Wolfgang

Subjects
JAK inhibition, rheumatoid arthritis, NK cells, synovial fibroblasts
Abstract

OBJECTIVE: Findings from recent transcriptome analyses of the synovium of patients with rheumatoid arthritis (RA) have revealed that 15-fold expanded HLA–DR+CD90+ synovial fibroblasts potentially act as key mediators of inflammation. The reasons for the expansion of HLA–DR+CD90+ synovial fibroblasts are unclear, but genetic signatures indicate that interferon-γ (IFNγ) plays a central role in the generation of this fibroblast subset. The present study was undertaken to investigate the generation, function and therapeutically intended blockage of HLA–DR+CD90+ synovial fibroblasts. METHODS: We combined functional assays using primary human materials and focused bioinformatic analyses of mass cytometry and transcriptomics patient data sets. RESULTS: We detected enriched and activated Fcγ receptor type IIIa–positive (CD16+) NK cells in the synovial tissue from patients with active RA. Soluble immune complexes were recognized by CD16 in a newly described reporter cell model, a mechanism that could be contributing to the activation of natural killer (NK) cells in RA. In vitro, NK cell–derived IFNγ induced HLA–DR on CD90+ synovial fibroblasts, leading to an inflammatory, cytokine-secreting HLA–DR+CD90+ phenotype. HLA–DR+CD90+ synovial fibroblasts consecutively activated CD4+ T cells upon receptor crosslinking via superantigens. HLA–DR+CD90+ synovial fibroblasts also activated CD4+ T cells in the absence of superantigens, an effect that was initiated by NK cell–derived IFNγ and that was 4 times stronger in patients with RA compared to patients with osteoarthritis. Finally, JAK inhibition in synovial fibroblasts prevented HLA–DR induction and blocked proinflammatory signals to T cells. CONCLUSION: The HLA–DR+CD90+ phenotype represents an activation state of synovial fibroblasts during the process of inflammation in RA that can be induced by IFNγ, likely generated from infiltrating leukocytes such as activated NK cells. The induction of these proinflammatory, interleukin-6–producing, and likely antigen-presenting synovial fibroblasts can be targeted by JAK inhibition.

Published
2021

69. Impact of Biological and Lifestyle Factors on Cognitive Aging and Work Ability in the Dortmund Vital Study: Protocol of an Interdisciplinary, Cross-sectional, and Longitudinal Study

Author

Gajewski, Patrick, Getzmann, Stephan, Bröde, Peter, Burke, Michael, Cadenas, Cristina, Capellino, Silvia, Claus, Maren, Genc, Erhan, Golka, Klaus, Hengstler, Jan, Kleinsorge, Thomas, Marchan, Rosemarie, Nitsche, Michael, Reinders, Joerg, van Thriel, Christoph, Watzl, Carsten, and Wascher, Edmund

Subjects
lifespan, cardiovascular system, neuropsychology, cognitive aging, genetic polymorphisms, biomarkers, aging, longitudinal study, metabolism, occupational health, longevity, electroencephalography, latent infections, magnetic resonance imaging, immunology, stress, lifestyle
Abstract

BACKGROUND: Previous research revealed several biological and environmental factors modulating cognitive functioning over a human’s lifespan. However, the relationships and interactions between biological factors (eg, genetic polymorphisms, immunological parameters, metabolic products, or infectious diseases) and environmental factors (eg, lifestyle, physical activity, nutrition, and work type or stress at work) as well as their impact on cognitive functions across the lifespan are still poorly understood with respect to their complexity. OBJECTIVE: The goal of the Dortmund Vital Study is to validate previous hypotheses as well as generate and validate new hypotheses about the relationships among aging, working conditions, genetic makeup, stress, metabolic functions, the cardiovascular system, the immune system, and mental performance over the human lifespan with a focus on healthy working adults. The Dortmund Vital Study is a multidisciplinary study involving the Departments of Ergonomics, Immunology, Psychology and Neurosciences, and Toxicology at the Leibniz Research Centre for Working Environment and Human Factors at the Technical University of Dortmund (IfADo) in Germany, as well as several national and international partners. METHODS: The Dortmund Vital Study is designed as a combined cross-sectional and longitudinal study. Approximately 600 healthy subjects aged between 20 and 70 years will participate. A wide range of demographic, psychological, behavioral, sensory, cardiovascular, immunological, and biochemical data, a comprehensive electroencephalography (EEG)-based cognitive test battery as well as structural and functional magnetic resonance imaging (MRI) have been included in the study. RESULTS: The study was approved by the Ethics Committee of IfADo in October 2015. The baseline testing was conducted between 2016 and 2021 and will be repeated every 5 years (3 follow-up measures until 2035). As of March 2020 (until the outbreak of the COVID-19 pandemic), 593 participants have been enrolled. Some results from the cross-sectional part of the study were already published, further results will be published soon. Longitudinal data will be analyzed and published by 2025. CONCLUSIONS: We anticipate that the study will shed light on sources of interindividual differences in the alterations of cognitive functioning with increasing age and reveal biological and lifestyle markers contributing to work ability, longevity, and healthy aging on the one hand, and to risk factors for cognitive decline, mild cognitive impairment, or even dementia on the other hand.

Published
2021

74. Immune response in ofatumumab treated multiple sclerosis patients aft er SARS-CoV-2 vaccination.

Author

Faissner, Simon, Heitmann, Neele, Plaza-Sirvent, Carlos, Trendelenburg, Paulina, Ceylan, Ulas, Motte, Jeremias, Bessen, Clara, Urlaub, Doris, Watzl, Carsten, Overheu, Oliver, Reinacher-Schick, Anke, Hellwig, Kerstin, Pfaender, Stephanie, Schmitz, Ingo, and Gold, Ralf

Subjects
IMMUNE response, HUMORAL immunity, REGULATORY T cells, MULTIPLE sclerosis, SARS-CoV-2
Abstract

Objective: The pandemic induced by SARS-CoV-2 has huge implications for patients with immunosuppression that is caused by disorders or specific treatments. Especially approaches targeting B cells via anti-CD20 therapy are associated with impaired humoral immune response but sustained cellular immunity. Ofatumumab is a human anti-CD20 directed antibody applied in low dosages subcutaneously, recently licensed for Multiple Sclerosis (MS). Effects of early ofatumumab treatment on alterations of immune cell composition and immune response towards SARS-CoV-2 are incompletely understood. Methods: We here investigated immune cell alterations in early ofatumumab (Ofa) treated patients and effects on humoral (titer, neutralization capacity against wild type, Delta and Omicron) and cellular immune responses in Ofa treated MS patients following a third vaccination against SARS-CoV-2 compared to healthy controls. Results: We show that a mean treatment duration of three months in the Ofa group led to near complete B cell depletion in line with altered composition of certain CD4+ T cell subpopulations such as enhanced frequencies of naive and a decrease of non-suppressive regulatory T cells (Tregs). Titer and neutralization capacity against SARS-CoV-2 variants was impaired while cellular immune response was sustained, characterized by a strong T helper 1 profile (Th1). Interpretation: In summary, low dosage ofatumumab treatment elicits sustained depletion of B cells in line with alterations of immune cells, mainly Tregs. This is associated with impaired humoral immune response towards SARS-CoV-2 vaccination but preserved, Th1 driven cellular immunity adding crucial information regarding early effects of low dosage anti-CD20 therapy on humoral and cellular immunity. [ABSTRACT FROM AUTHOR]

Published
2022
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75. COVID-19 progression is potentially driven by T cell immunopathogenesis

Author

Anft, Moritz, Paniskaki, Krystallenia, Blazquez-Navarro, Arturo, Doevelaar, Adrian Atila Nicolas, Seibert, Felix, Hoelzer, Bodo, Skrzypczyk, Sarah, Kohut, Eva, Kurek, Julia, Zapka, Jan, Wehler, Patrizia, Kaliszczyk, Sviatlana, Bajda, Sharon, Thieme, Constantin, Roch, Toralf, Konik, Margarethe Justine, Brenner, Thorsten, Tempfer, Clemens, Watzl, Carsten, Dolff, Sebastian, Dittmer, Ulf, Westhoff, Timm, Witzke, Oliver, Stervbo, Ulrik, and Babel, Nina

Abstract

Background: The role of cellular immunity in pathogenesis of COVID-19 is unclear and conflicting data points to insufficient or pathogenic immunity as drivers of COVID-19 progression. Here we aimed to delineate the phenotype and function of the immune system in patients with moderate, severe, and critical COVID-19. Methods: In this prospective study, we included 53 patients with moderate (n=21), severe (n=18), and critical (n=14) COVID-19 manifestations. Using multiparametric flow cytometry we compared quantitative, phenotypic, and functional characteristics of circulating immune cells, SARS-CoV-2 antigen-reactive T-cells, and humoral immunity. Results: Deep phenotypic profiling revealed a depletion of circulating bulk CD8+ T-cells, CD4+ and CD8+ T-cell subsets with activated memory/effector T-cells expressing CD57+, HLA-DR+, and the key activation and migration molecule CD11a++ in critical COVID-19. Importantly, survival from acute respiratory distress syndrome was accompanied by a recovery of the depleted CD11++ T-cell subsets including T-cells expressing CD28, CD57, HLA-DR activation/effector molecules. We further observed a stronger response of S-protein specific T-cells producing inflammatory cytokines in critical COVID-19 cases. This seemingly contradictory observation is in fact confirmation of the underlying immunopathogenesis in patients with critical COVID-19. Conclusion: Our findings suggest a CD11a-based immune signature as a possible prognostic marker for disease development. Our data further reveal that increased rather than decreased SARS-CoV-2 specific T cell immunity is associated with adverse outcome in COVID-19. Tissue migration of activated effectors T-cells may constitute a crucial cornerstone in the immunopathogenesis of SARS-CoV-2 associated tissue injury.

Published
2020
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81. COVID-19-Induced ARDS Is Associated with Decreased Frequency of Activated Memory/Effector T Cells Expressing CD11a++

Author

Anft, Moritz, primary, Paniskaki, Krystallenia, additional, Blazquez-Navarro, Arturo, additional, Doevelaar, Adrian, additional, Seibert, Felix S., additional, Hölzer, Bodo, additional, Skrzypczyk, Sarah, additional, Kohut, Eva, additional, Kurek, Julia, additional, Zapka, Jan, additional, Wehler, Patrizia, additional, Kaliszczyk, Sviatlana, additional, Bajda, Sharon, additional, Thieme, Constantin J., additional, Roch, Toralf, additional, Konik, Margarethe Justine, additional, Berger, Marc Moritz, additional, Brenner, Thorsten, additional, Kölsch, Uwe, additional, Meister, Toni L., additional, Pfaender, Stephanie, additional, Steinmann, Eike, additional, Tempfer, Clemens, additional, Watzl, Carsten, additional, Dolff, Sebastian, additional, Dittmer, Ulf, additional, Abou-El-Enein, Mohamed, additional, Westhoff, Timm H., additional, Witzke, Oliver, additional, Stervbo, Ulrik, additional, and Babel, Nina, additional

Published
2020
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82. Effect of JAK Inhibition on the Induction of Proinflammatory HLA–DR+CD90+ Rheumatoid Arthritis Synovial Fibroblasts by Interferon‐γ.

Author

Zhao, Shuyang, Grieshaber‐Bouyer, Ricardo, Rao, Deepak A., Kolb, Philipp, Chen, Haizhang, Andreeva, Ivana, Tretter, Theresa, Lorenz, Hanns‐Martin, Watzl, Carsten, Wabnitz, Guido, Tykocinski, Lars‐Oliver, and Merkt, Wolfgang

Subjects
FLOW cytometry, INTERLEUKINS, FIBROBLASTS, CELL culture, JANUS kinases, BIOINFORMATICS, RHEUMATOID arthritis, GENE expression profiling, INFLAMMATORY mediators, T cells, PHENOTYPES, SYNOVIAL fluid
Abstract

Objective: Findings from recent transcriptome analyses of the synovium of patients with rheumatoid arthritis (RA) have revealed that 15‐fold expanded HLA–DR+CD90+ synovial fibroblasts potentially act as key mediators of inflammation. The reasons for the expansion of HLA–DR+CD90+ synovial fibroblasts are unclear, but genetic signatures indicate that interferon‐γ (IFNγ) plays a central role in the generation of this fibroblast subset. The present study was undertaken to investigate the generation, function and therapeutically intended blockage of HLA–DR+CD90+ synovial fibroblasts. Methods: We combined functional assays using primary human materials and focused bioinformatic analyses of mass cytometry and transcriptomics patient data sets. Results: We detected enriched and activated Fcγ receptor type IIIa–positive (CD16+) NK cells in the synovial tissue from patients with active RA. Soluble immune complexes were recognized by CD16 in a newly described reporter cell model, a mechanism that could be contributing to the activation of natural killer (NK) cells in RA. In vitro, NK cell–derived IFNγ induced HLA–DR on CD90+ synovial fibroblasts, leading to an inflammatory, cytokine‐secreting HLA–DR+CD90+ phenotype. HLA–DR+CD90+ synovial fibroblasts consecutively activated CD4+ T cells upon receptor crosslinking via superantigens. HLA–DR+CD90+ synovial fibroblasts also activated CD4+ T cells in the absence of superantigens, an effect that was initiated by NK cell–derived IFNγ and that was 4 times stronger in patients with RA compared to patients with osteoarthritis. Finally, JAK inhibition in synovial fibroblasts prevented HLA–DR induction and blocked proinflammatory signals to T cells. Conclusion: The HLA–DR+CD90+ phenotype represents an activation state of synovial fibroblasts during the process of inflammation in RA that can be induced by IFNγ, likely generated from infiltrating leukocytes such as activated NK cells. The induction of these proinflammatory, interleukin‐6–producing, and likely antigen‐presenting synovial fibroblasts can be targeted by JAK inhibition. [ABSTRACT FROM AUTHOR]

Published
2022
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86. Activating NK- receptors, homing selectins and inhibitory Siglecs recognize EBOLA-GP and HPV-L1NK

Author

Jarahian, Mostafa, primary, Marstaller, Katharina, additional, Wurmbäck, Heribert, additional, Banna, Nadine, additional, Ahani, Roshanak, additional, Etemadzadeh, Hossein, additional, Boller, Lea Katharina, additional, Azadmanesh, Kayhan, additional, Cid-Arregui, Angel, additional, Berger, Martin R, additional, Momburg, Frank, additional, and Watzl, Carsten, additional

Published
2020
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87. The SARS-CoV-2 T-cell immunity is directed against the spike, membrane, and nucleocapsid protein and associated with COVID 19 severity

Author

Thieme, Constantin J, primary, Anft, Moritz, additional, Paniskaki, Krystallenia, additional, Blazquez-Navarro, Arturo, additional, Doevelaar, Adrian, additional, Seibert, Felix S, additional, Hoelzer, Bodo, additional, Konik, Margarethe Justine, additional, Brenner, Thorsten, additional, Tempfer, Clemens, additional, Watzl, Carsten, additional, Dolff, Sebastian, additional, Dittmer, Ulf, additional, Westhoff, Timm H., additional, Witzke, Oliver, additional, Stervbo, Ulrik, additional, Roch, Toralf, additional, and Babel, Nina, additional

Published
2020
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88. A possible role of immunopathogenesis in COVID-19 progression

Author

Anft, Moritz, primary, Paniskaki, Krystallenia, additional, Blazquez-Navarro, Arturo, additional, Doevelaar, Adrian, additional, Seibert, Felix S., additional, Hoelzer, Bodo, additional, Skrzypczyk, Sarah, additional, Kohut, Eva, additional, Kurek, Julia, additional, Zapka, Jan, additional, Wehler, Patrizia, additional, Kaliszczyk, Sviatlana, additional, Bajda, Sharon, additional, Thieme, Constantin J., additional, Roch, Toralf, additional, Justine Konik, Margarethe, additional, Brenner, Thorsten, additional, Tempfer, Clemens, additional, Watzl, Carsten, additional, Dolff, Sebastian, additional, Dittmer, Ulf, additional, Westhoff, Timm H., additional, Witzke, Oliver, additional, Stervbo, Ulrik, additional, and Babel, Nina, additional

Published
2020
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90. The SARS-COV-2 T-Cell Immunity is Directed Against the Spike, Membrane, and Nucleocapsid Protein and Associated with COVID 19 Severity

Author

Thieme, Constantin, primary, Anft, Moritz, additional, Paniskaki, Krystallenia, additional, Blázquez Navarro, Arturo, additional, Doevelaar, Adrian, additional, Seibert, Felix S., additional, Hölzer, Bodo, additional, Konik, Margarethe Justine, additional, Brenner, Thorsten, additional, Tempfer, Clemens, additional, Watzl, Carsten, additional, Dolff, Sebastian, additional, Dittmer, Ulf, additional, Witzke, Oliver, additional, Westhoff, Timm H., additional, Stervbo, Ulrik, additional, Roch, Toralf, additional, and Babel, Nina, additional

Published
2020
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93. Circulating growth/differentiation factor 15 is associated with human CD56 natural killer cell dysfunction and nosocomial infection in severe systemic inflammation

Author

Kleinertz, Holger, Hepner-Schefczyk, Monika, Ehnert, Sabrina, Claus, Maren, Halbgebauer, Rebecca, Boller, Lea, Huber-Lang, Markus, Cinelli, Paolo, Kirschning, Carsten, Flohé, Sascha, Sander, André, Waydhas, Christian, Vonderhagen, Sonja, Jäger, Marcus, Dudda, Marcel, Watzl, Carsten, Flohé, Stefanie B, University of Zurich, and Flohé, Stefanie B

Subjects
10021 Department of Trauma Surgery, 1300 General Biochemistry, Genetics and Molecular Biology, 610 Medicine & health
Published
2019

94. NK cells from patients with rheumatic disease specifically react in response to rituximab

Author

Merkt, Wolfgang, Zhao, Shuyang, Blank, Norbert, Watzl, Carsten, and Lorenz, Hanns-Martin

Subjects
ddc: 610, immune system diseases, hemic and lymphatic diseases, 610 Medical sciences, Medicine
Abstract

Background: The monoclonal anti-CD20 antibody rituximab is successfully used in the treatment of numerous rheumatic diseases. In vivo, rituximab leads to the depletion of B lymphocytes. Natural killer (NK) cells can kill rituximab-coated tumor cells [ref:1]. Using an NK cell depletion and [for full text, please go to the a.m. URL], 46. Kongress der Deutschen Gesellschaft für Rheumatologie (DGRh), 32. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh), Wissenschaftliche Herbsttagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR)

Published
2019
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96. LIPG-promoted lipid storage mediates adaptation to oxidative stress in breast cancer

Author

Cadenas, Cristina, Vosbeck, Sonja, Edlund, Karolina, Grgas, Katharina, Madjar, Katrin, Hellwig, Birte, Adawy, Alshaimaa, Glotzbach, Annika, Stewart, Joanna D., Lesjak, Michaela S., Franckenstein, Dennis, Claus, Maren, Hayen, Heiko, Schriewer, Alexander, Gianmoena, Kathrin, Thaler, Sonja, Schmidt, Marcus, Micke, Patrick, Pontén, Fredrik, Mardinoglu, Adil, Zhang, Cheng, Käfferlein, Heiko U., Watzl, Carsten, Frank, Saša, Rahnenführer, Jörg, Marchan, Rosemarie, Hengstler, Jan G., Cadenas, Cristina, Vosbeck, Sonja, Edlund, Karolina, Grgas, Katharina, Madjar, Katrin, Hellwig, Birte, Adawy, Alshaimaa, Glotzbach, Annika, Stewart, Joanna D., Lesjak, Michaela S., Franckenstein, Dennis, Claus, Maren, Hayen, Heiko, Schriewer, Alexander, Gianmoena, Kathrin, Thaler, Sonja, Schmidt, Marcus, Micke, Patrick, Pontén, Fredrik, Mardinoglu, Adil, Zhang, Cheng, Käfferlein, Heiko U., Watzl, Carsten, Frank, Saša, Rahnenführer, Jörg, Marchan, Rosemarie, and Hengstler, Jan G.

Abstract

Endothelial lipase (LIPG) is a cell surface associated lipase that displays phospholipase A1 activity towards phosphatidylcholine present in high‐density lipoproteins (HDL). LIPG was recently reported to be expressed in breast cancer and to support proliferation, tumourigenicity and metastasis. Here we show that severe oxidative stress leading to AMPK activation triggers LIPG upregulation, resulting in intracellular lipid droplet accumulation in breast cancer cells, which supports survival. Neutralizing oxidative stress abrogated LIPG upregulation and the concomitant lipid storage. In human breast cancer, high LIPG expression was observed in a limited subset of tumours and was significantly associated with shorter metastasis‐free survival in node‐negative, untreated patients. Moreover, expression of PLIN2 and TXNRD1 in these tumours indicated a link to lipid storage and oxidative stress. Altogether, our findings reveal a previously unrecognized role for LIPG in enabling oxidative stress‐induced lipid droplet accumulation in tumour cells that protects against oxidative stress, and thus supports tumour progression.

Published
2019
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97. NK cells switch from granzyme B to death receptor–mediated cytotoxicity during serial killing

Author

Prager, Isabel, Liesche, Clarissa, van Ooijen, Hanna, Urlaub, Doris, Verron, Quentin, Sandström, Niklas, Fasbender, Frank, Claus, Maren, Eils, Roland, Beaudouin, Joël, Önfelt, Björn, Watzl, Carsten, Prager, Isabel, Liesche, Clarissa, van Ooijen, Hanna, Urlaub, Doris, Verron, Quentin, Sandström, Niklas, Fasbender, Frank, Claus, Maren, Eils, Roland, Beaudouin, Joël, Önfelt, Björn, and Watzl, Carsten

Abstract

NK cells eliminate virus-infected and tumor cells by releasing cytotoxic granules containing granzyme B (GrzB) or by engaging death receptors that initiate caspase cascades. The orchestrated interplay between both cell death pathways remains poorly defined. Here we simultaneously measure the activities of GrzB and caspase-8 in tumor cells upon contact with human NK cells. We observed that NK cells switch from inducing a fast GrzB-mediated cell death in their first killing events to a slow death receptor–mediated killing during subsequent tumor cell encounters. Target cell contact reduced intracellular GrzB and perforin and increased surface-CD95L in NK cells over time, showing how the switch in cytotoxicity pathways is controlled. Without perforin, NK cells were unable to perform GrzB-mediated serial killing and only killed once via death receptors. In contrast, the absence of CD95 on tumor targets did not impair GrzB-mediated serial killing. This demonstrates that GrzB and death receptor–mediated cytotoxicity are differentially regulated during NK cell serial killing., QC 20190822

Published
2019
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98. Guidelines for the use of flow cytometry and cell sorting in immunological studies (second edition)

Author

Cossarizza, Andrea, Chang, Hyun-Dong, Radbruch, Andreas, Acs, Andreas, Adam, Dieter, Adam-Klages, Sabine, Agace, William W., Aghaeepour, Nima, Akdis, Muebeccel, Allez, Matthieu, Almeida, Larissa Nogueira, Alvisi, Giorgia, Anderson, Graham, Andrae, Immanuel, Annunziato, Francesco, Anselmo, Achille, Bacher, Petra, Baldari, Cosima T., Bari, Sudipto, Barnaba, Vincenzo, Barros-Martins, Joana, Battistini, Luca, Bauer, Wolfgang, Baumgart, Sabine, Baumgarth, Nicole, Baumjohann, Dirk, Baying, Bianka, Bebawy, Mary, Becher, Burkhard, Beisker, Wolfgang, Benes, Vladimir, Beyaert, Rudi, Blanco, Alfonso, Boardman, Dominic A., Bogdan, Christian, Borger, Jessica G., Borsellino, Giovanna, Boulais, Philip E., Bradford, Jolene A., Brenner, Dirk, Brinkman, Ryan R., Brooks, Anna E. S., Busch, Dirk H., Buescher, Martin, Bushnell, Timothy P., Calzetti, Federica, Cameron, Garth, Cammarata, Ilenia, Cao, Xuetao, Cardell, Susanna L., Casola, Stefano, Cassatella, Marco A., Cavani, Andrea, Celada, Antonio, Chatenoud, Lucienne, Chattopadhyay, Pratip K., Chow, Sue, Christakou, Eleni, Cicin-Sain, Luka, Clerici, Mario, Colombo, Federico S., Cook, Laura, Cooke, Anne, Cooper, Andrea M., Corbett, Alexandra J., Cosma, Antonio, Cosmi, Lorenzo, Coulie, Pierre G., Cumano, Ana, Cvetkovic, Ljiljana, Dang, Van Duc, Dang-Heine, Chantip, Davey, Martin S., Davies, Derek, De Biasi, Sara, Del Zotto, Genny, Dela Cruz, Gelo Victoriano, Delacher, Michael, Della Bella, Silvia, Dellabona, Paolo, Deniz, Guennur, Dessing, Mark, Di Santo, James P., Diefenbach, Andreas, Dieli, Francesco, Dolf, Andreas, Doerner, Thomas, Dress, Regine J., Dudziak, Diana, Dustin, Michael, Dutertre, Charles-Antoine, Ebner, Friederike, Eckle, Sidonia B. G., Edinger, Matthias, Eede, Pascale, Ehrhardt, Goetz R. A., Eich, Marcus, Engel, Pablo, Engelhardt, Britta, Erdei, Anna, Esser, Charlotte, Everts, Bart, Evrard, Maximilien, Falk, Christine S., Fehniger, Todd A., Felipo-Benavent, Mar, Ferry, Helen, Feuerer, Markus, Filby, Andrew, Filkor, Kata, Fillatreau, Simon, Follo, Marie, Foerster, Irmgard, Foster, John, Foulds, Gemma A., Frehse, Britta, Frenette, Paul S., Frischbutter, Stefan, Fritzsche, Wolfgang, Galbraith, David W., Gangaev, Anastasia, Garbi, Natalio, Gaudilliere, Brice, Gazzinelli, Ricardo T., Geginat, Jens, Gerner, Wilhelm, Gherardin, Nicholas A., Ghoreschi, Kamran, Gibellini, Lara, Ginhoux, Florent, Goda, Keisuke, Godfrey, Dale I., Goettlinger, Christoph, Gonzalez-Navajas, Jose M., Goodyear, Carl S., Gori, Andrea, Grogan, Jane L., Grummitt, Daryl, Gruetzkau, Andreas, Haftmann, Claudia, Hahn, Jonas, Hammad, Hamida, Haemmerling, Guenter, Hansmann, Leo, Hansson, Goran, Harpur, Christopher M., Hartmann, Susanne, Hauser, Andrea, Hauser, Anja E., Haviland, David L., Hedley, David, Hernandez, Daniela C., Herrera, Guadalupe, Herrmann, Martin, Hess, Christoph, Hoefer, Thomas, Hoffmann, Petra, Hogquist, Kristin, Holland, Tristan, Hollt, Thomas, Holmdahl, Rikard, Hombrink, Pleun, Houston, Jessica P., Hoyer, Bimba F., Huang, Bo, Huang, Fang-Ping, Huber, Johanna E., Huehn, Jochen, Hundemer, Michael, Hunter, Christopher A., Hwang, William Y. K., Iannone, Anna, Ingelfinger, Florian, Ivison, Sabine M., Jaeck, Hans-Martin, Jani, Peter K., Javega, Beatriz, Jonjic, Stipan, Kaiser, Toralf, Kalina, Tomas, Kamradt, Thomas, Kaufmann, Stefan H. E., Keller, Baerbel, Ketelaars, Steven L. C., Khalilnezhad, Ahad, Khan, Srijit, Kisielow, Jan, Klenerman, Paul, Knopf, Jasmin, Koay, Hui-Fern, Kobow, Katja, Kolls, Jay K., Kong, Wan Ting, Kopf, Manfred, Korn, Thomas, Kriegsmann, Katharina, Kristyanto, Hendy, Kroneis, Thomas, Krueger, Andreas, Kuehne, Jenny, Kukat, Christian, Kunkel, Desiree, Kunze-Schumacher, Heike, Kurosaki, Tomohiro, Kurts, Christian, Kvistborg, Pia, Kwok, Immanuel, Landry, Jonathan, Lantz, Olivier, Lanuti, Paola, LaRosa, Francesca, Lehuen, Agnes, LeibundGut-Landmann, Salome, Leipold, Michael D., Leung, Leslie Y. T., Levings, Megan K., Lino, Andreia C., Liotta, Francesco, Litwin, Virginia, Liu, Yanling, Ljunggren, Hans-Gustaf, Lohoff, Michael, Lombardi, Giovanna, Lopez, Lilly, Lopez-Botet, Miguel, Lovett-Racke, Amy E., Lubberts, Erik, Luche, Herve, Ludewig, Burkhard, Lugli, Enrico, Lunemann, Sebastian, Maecker, Holden T., Maggi, Laura, Maguire, Orla, Mair, Florian, Mair, Kerstin H., Mantovani, Alberto, Manz, Rudolf A., Marshall, Aaron J., Martinez-Romero, Alicia, Martrus, Gloria, Marventano, Ivana, Maslinski, Wlodzimierz, Matarese, Giuseppe, Mattioli, Anna Vittoria, Maueroder, Christian, Mazzoni, Alessio, McCluskey, James, McGrath, Mairi, McGuire, Helen M., McInnes, Iain B., Mei, Henrik E., Melchers, Fritz, Melzer, Susanne, Mielenz, Dirk, Miller, Stephen D., Mills, Kingston H. G., Minderman, Hans, Mjosberg, Jenny, Moore, Jonni, Moran, Barry, Moretta, Lorenzo, Mosmann, Tim R., Mueller, Susann, Multhoff, Gabriele, Munoz, Luis Enrique, Munz, Christian, Nakayama, Toshinori, Nasi, Milena, Neumann, Katrin, Ng, Lai Guan, Niedobitek, Antonia, Nourshargh, Sussan, Nunez, Gabriel, O'Connor, Jose-Enrique, Ochel, Aaron, Oja, Anna, Ordonez, Diana, Orfao, Alberto, Orlowski-Oliver, Eva, Ouyang, Wenjun, Oxenius, Annette, Palankar, Raghavendra, Panse, Isabel, Pattanapanyasat, Kovit, Paulsen, Malte, Pavlinic, Dinko, Penter, Livius, Peterson, Paert, Peth, Christian, Petriz, Jordi, Piancone, Federica, Pickl, Winfried F., Piconese, Silvia, Pinti, Marcello, Pockley, A. Graham, Podolska, Malgorzata Justyna, Poon, Zhiyong, Pracht, Katharina, Prinz, Immo, Pucillo, Carlo E. M., Quataert, Sally A., Quatrini, Linda, Quinn, Kylie M., Radbruch, Helena, Radstake, Tim R. D. J., Rahmig, Susann, Rahn, Hans-Peter, Rajwa, Bartek, Ravichandran, Gevitha, Raz, Yotam, Rebhahn, Jonathan A., Recktenwald, Diether, Reimer, Dorothea, Reis e Sousa, Caetano, Remmerswaal, Ester B. M., Richter, Lisa, Rico, Laura G., Riddell, Andy, Rieger, Aja M., Robinson, J. Paul, Romagnani, Chiara, Rubartelli, Anna, Ruland, Juergen, Saalmueller, Armin, Saeys, Yvan, Saito, Takashi, Sakaguchi, Shimon, Sala-de-Oyanguren, Francisco, Samstag, Yvonne, Sanderson, Sharon, Sandrock, Inga, Santoni, Angela, Sanz, Ramon Bellmas, Saresella, Marina, Sautes-Fridman, Catherine, Sawitzki, Birgit, Schadt, Linda, Scheffold, Alexander, Scherer, Hans U., Schiemann, Matthias, Schildberg, Frank A., Schimisky, Esther, Schlitzer, Andreas, Schlosser, Josephine, Schmid, Stephan, Schmitt, Steffen, Schober, Kilian, Schraivogel, Daniel, Schuh, Wolfgang, Schueler, Thomas, Schulte, Reiner, Schulz, Axel Ronald, Schulz, Sebastian R., Scotta, Cristiano, Scott-Algara, Daniel, Sester, David P., Shankey, T. Vincent, Silva-Santos, Bruno, Simon, Anna Katharina, Sitnik, Katarzyna M., Sozzani, Silvano, Speiser, Daniel E., Spidlen, Josef, Stahlberg, Anders, Stall, Alan M., Stanley, Natalie, Stark, Regina, Stehle, Christina, Steinmetz, Tobit, Stockinger, Hannes, Takahama, Yousuke, Takeda, Kiyoshi, Tan, Leonard, Tarnok, Attila, Tiegs, Gisa, Toldi, Gergely, Tornack, Julia, Traggiai, Elisabetta, Trebak, Mohamed, Tree, Timothy I. M., Trotter, Joe, Trowsdale, John, Tsoumakidou, Maria, Ulrich, Henning, Urbanczyk, Sophia, van de Veen, Willem, van den Broek, Maries, van der Pol, Edwin, Van Gassen, Sofie, Van Isterdael, Gert, van Lier, Rene A. W., Veldhoen, Marc, Vento-Asturias, Salvador, Vieira, Paulo, Voehringer, David, Volk, Hans-Dieter, von Borstel, Anouk, von Volkmann, Konrad, Waisman, Ari, Walker, Rachael V., Wallace, Paul K., Wang, Sa A., Wang, Xin M., Ward, Michael D., Ward-Hartstonge, Kirsten A., Warnatz, Klaus, Warnes, Gary, Warth, Sarah, Waskow, Claudia, Watson, James V., Watzl, Carsten, Wegener, Leonie, Weisenburger, Thomas, Wiedemann, Annika, Wienands, Juergen, Wilharm, Anneke, Wilkinson, Robert John, Willimsky, Gerald, Wing, James B., Winkelmann, Rieke, Winkler, Thomas H., Wirz, Oliver F., Wong, Alicia, Wurst, Peter, Yang, Jennie H. M., Yang, Juhao, Yazdanbakhsh, Maria, Yu, Liping, Yue, Alice, Zhang, Hanlin, Zhao, Yi, Ziegler, Susanne Maria, Zielinski, Christina, Zimmermann, Jakob, Zychlinsky, Arturo, Cossarizza, Andrea, Chang, Hyun-Dong, Radbruch, Andreas, Acs, Andreas, Adam, Dieter, Adam-Klages, Sabine, Agace, William W., Aghaeepour, Nima, Akdis, Muebeccel, Allez, Matthieu, Almeida, Larissa Nogueira, Alvisi, Giorgia, Anderson, Graham, Andrae, Immanuel, Annunziato, Francesco, Anselmo, Achille, Bacher, Petra, Baldari, Cosima T., Bari, Sudipto, Barnaba, Vincenzo, Barros-Martins, Joana, Battistini, Luca, Bauer, Wolfgang, Baumgart, Sabine, Baumgarth, Nicole, Baumjohann, Dirk, Baying, Bianka, Bebawy, Mary, Becher, Burkhard, Beisker, Wolfgang, Benes, Vladimir, Beyaert, Rudi, Blanco, Alfonso, Boardman, Dominic A., Bogdan, Christian, Borger, Jessica G., Borsellino, Giovanna, Boulais, Philip E., Bradford, Jolene A., Brenner, Dirk, Brinkman, Ryan R., Brooks, Anna E. S., Busch, Dirk H., Buescher, Martin, Bushnell, Timothy P., Calzetti, Federica, Cameron, Garth, Cammarata, Ilenia, Cao, Xuetao, Cardell, Susanna L., Casola, Stefano, Cassatella, Marco A., Cavani, Andrea, Celada, Antonio, Chatenoud, Lucienne, Chattopadhyay, Pratip K., Chow, Sue, Christakou, Eleni, Cicin-Sain, Luka, Clerici, Mario, Colombo, Federico S., Cook, Laura, Cooke, Anne, Cooper, Andrea M., Corbett, Alexandra J., Cosma, Antonio, Cosmi, Lorenzo, Coulie, Pierre G., Cumano, Ana, Cvetkovic, Ljiljana, Dang, Van Duc, Dang-Heine, Chantip, Davey, Martin S., Davies, Derek, De Biasi, Sara, Del Zotto, Genny, Dela Cruz, Gelo Victoriano, Delacher, Michael, Della Bella, Silvia, Dellabona, Paolo, Deniz, Guennur, Dessing, Mark, Di Santo, James P., Diefenbach, Andreas, Dieli, Francesco, Dolf, Andreas, Doerner, Thomas, Dress, Regine J., Dudziak, Diana, Dustin, Michael, Dutertre, Charles-Antoine, Ebner, Friederike, Eckle, Sidonia B. G., Edinger, Matthias, Eede, Pascale, Ehrhardt, Goetz R. A., Eich, Marcus, Engel, Pablo, Engelhardt, Britta, Erdei, Anna, Esser, Charlotte, Everts, Bart, Evrard, Maximilien, Falk, Christine S., Fehniger, Todd A., Felipo-Benavent, Mar, Ferry, Helen, Feuerer, Markus, Filby, Andrew, Filkor, Kata, Fillatreau, Simon, Follo, Marie, Foerster, Irmgard, Foster, John, Foulds, Gemma A., Frehse, Britta, Frenette, Paul S., Frischbutter, Stefan, Fritzsche, Wolfgang, Galbraith, David W., Gangaev, Anastasia, Garbi, Natalio, Gaudilliere, Brice, Gazzinelli, Ricardo T., Geginat, Jens, Gerner, Wilhelm, Gherardin, Nicholas A., Ghoreschi, Kamran, Gibellini, Lara, Ginhoux, Florent, Goda, Keisuke, Godfrey, Dale I., Goettlinger, Christoph, Gonzalez-Navajas, Jose M., Goodyear, Carl S., Gori, Andrea, Grogan, Jane L., Grummitt, Daryl, Gruetzkau, Andreas, Haftmann, Claudia, Hahn, Jonas, Hammad, Hamida, Haemmerling, Guenter, Hansmann, Leo, Hansson, Goran, Harpur, Christopher M., Hartmann, Susanne, Hauser, Andrea, Hauser, Anja E., Haviland, David L., Hedley, David, Hernandez, Daniela C., Herrera, Guadalupe, Herrmann, Martin, Hess, Christoph, Hoefer, Thomas, Hoffmann, Petra, Hogquist, Kristin, Holland, Tristan, Hollt, Thomas, Holmdahl, Rikard, Hombrink, Pleun, Houston, Jessica P., Hoyer, Bimba F., Huang, Bo, Huang, Fang-Ping, Huber, Johanna E., Huehn, Jochen, Hundemer, Michael, Hunter, Christopher A., Hwang, William Y. K., Iannone, Anna, Ingelfinger, Florian, Ivison, Sabine M., Jaeck, Hans-Martin, Jani, Peter K., Javega, Beatriz, Jonjic, Stipan, Kaiser, Toralf, Kalina, Tomas, Kamradt, Thomas, Kaufmann, Stefan H. E., Keller, Baerbel, Ketelaars, Steven L. C., Khalilnezhad, Ahad, Khan, Srijit, Kisielow, Jan, Klenerman, Paul, Knopf, Jasmin, Koay, Hui-Fern, Kobow, Katja, Kolls, Jay K., Kong, Wan Ting, Kopf, Manfred, Korn, Thomas, Kriegsmann, Katharina, Kristyanto, Hendy, Kroneis, Thomas, Krueger, Andreas, Kuehne, Jenny, Kukat, Christian, Kunkel, Desiree, Kunze-Schumacher, Heike, Kurosaki, Tomohiro, Kurts, Christian, Kvistborg, Pia, Kwok, Immanuel, Landry, Jonathan, Lantz, Olivier, Lanuti, Paola, LaRosa, Francesca, Lehuen, Agnes, LeibundGut-Landmann, Salome, Leipold, Michael D., Leung, Leslie Y. T., Levings, Megan K., Lino, Andreia C., Liotta, Francesco, Litwin, Virginia, Liu, Yanling, Ljunggren, Hans-Gustaf, Lohoff, Michael, Lombardi, Giovanna, Lopez, Lilly, Lopez-Botet, Miguel, Lovett-Racke, Amy E., Lubberts, Erik, Luche, Herve, Ludewig, Burkhard, Lugli, Enrico, Lunemann, Sebastian, Maecker, Holden T., Maggi, Laura, Maguire, Orla, Mair, Florian, Mair, Kerstin H., Mantovani, Alberto, Manz, Rudolf A., Marshall, Aaron J., Martinez-Romero, Alicia, Martrus, Gloria, Marventano, Ivana, Maslinski, Wlodzimierz, Matarese, Giuseppe, Mattioli, Anna Vittoria, Maueroder, Christian, Mazzoni, Alessio, McCluskey, James, McGrath, Mairi, McGuire, Helen M., McInnes, Iain B., Mei, Henrik E., Melchers, Fritz, Melzer, Susanne, Mielenz, Dirk, Miller, Stephen D., Mills, Kingston H. G., Minderman, Hans, Mjosberg, Jenny, Moore, Jonni, Moran, Barry, Moretta, Lorenzo, Mosmann, Tim R., Mueller, Susann, Multhoff, Gabriele, Munoz, Luis Enrique, Munz, Christian, Nakayama, Toshinori, Nasi, Milena, Neumann, Katrin, Ng, Lai Guan, Niedobitek, Antonia, Nourshargh, Sussan, Nunez, Gabriel, O'Connor, Jose-Enrique, Ochel, Aaron, Oja, Anna, Ordonez, Diana, Orfao, Alberto, Orlowski-Oliver, Eva, Ouyang, Wenjun, Oxenius, Annette, Palankar, Raghavendra, Panse, Isabel, Pattanapanyasat, Kovit, Paulsen, Malte, Pavlinic, Dinko, Penter, Livius, Peterson, Paert, Peth, Christian, Petriz, Jordi, Piancone, Federica, Pickl, Winfried F., Piconese, Silvia, Pinti, Marcello, Pockley, A. Graham, Podolska, Malgorzata Justyna, Poon, Zhiyong, Pracht, Katharina, Prinz, Immo, Pucillo, Carlo E. M., Quataert, Sally A., Quatrini, Linda, Quinn, Kylie M., Radbruch, Helena, Radstake, Tim R. D. J., Rahmig, Susann, Rahn, Hans-Peter, Rajwa, Bartek, Ravichandran, Gevitha, Raz, Yotam, Rebhahn, Jonathan A., Recktenwald, Diether, Reimer, Dorothea, Reis e Sousa, Caetano, Remmerswaal, Ester B. M., Richter, Lisa, Rico, Laura G., Riddell, Andy, Rieger, Aja M., Robinson, J. Paul, Romagnani, Chiara, Rubartelli, Anna, Ruland, Juergen, Saalmueller, Armin, Saeys, Yvan, Saito, Takashi, Sakaguchi, Shimon, Sala-de-Oyanguren, Francisco, Samstag, Yvonne, Sanderson, Sharon, Sandrock, Inga, Santoni, Angela, Sanz, Ramon Bellmas, Saresella, Marina, Sautes-Fridman, Catherine, Sawitzki, Birgit, Schadt, Linda, Scheffold, Alexander, Scherer, Hans U., Schiemann, Matthias, Schildberg, Frank A., Schimisky, Esther, Schlitzer, Andreas, Schlosser, Josephine, Schmid, Stephan, Schmitt, Steffen, Schober, Kilian, Schraivogel, Daniel, Schuh, Wolfgang, Schueler, Thomas, Schulte, Reiner, Schulz, Axel Ronald, Schulz, Sebastian R., Scotta, Cristiano, Scott-Algara, Daniel, Sester, David P., Shankey, T. Vincent, Silva-Santos, Bruno, Simon, Anna Katharina, Sitnik, Katarzyna M., Sozzani, Silvano, Speiser, Daniel E., Spidlen, Josef, Stahlberg, Anders, Stall, Alan M., Stanley, Natalie, Stark, Regina, Stehle, Christina, Steinmetz, Tobit, Stockinger, Hannes, Takahama, Yousuke, Takeda, Kiyoshi, Tan, Leonard, Tarnok, Attila, Tiegs, Gisa, Toldi, Gergely, Tornack, Julia, Traggiai, Elisabetta, Trebak, Mohamed, Tree, Timothy I. M., Trotter, Joe, Trowsdale, John, Tsoumakidou, Maria, Ulrich, Henning, Urbanczyk, Sophia, van de Veen, Willem, van den Broek, Maries, van der Pol, Edwin, Van Gassen, Sofie, Van Isterdael, Gert, van Lier, Rene A. W., Veldhoen, Marc, Vento-Asturias, Salvador, Vieira, Paulo, Voehringer, David, Volk, Hans-Dieter, von Borstel, Anouk, von Volkmann, Konrad, Waisman, Ari, Walker, Rachael V., Wallace, Paul K., Wang, Sa A., Wang, Xin M., Ward, Michael D., Ward-Hartstonge, Kirsten A., Warnatz, Klaus, Warnes, Gary, Warth, Sarah, Waskow, Claudia, Watson, James V., Watzl, Carsten, Wegener, Leonie, Weisenburger, Thomas, Wiedemann, Annika, Wienands, Juergen, Wilharm, Anneke, Wilkinson, Robert John, Willimsky, Gerald, Wing, James B., Winkelmann, Rieke, Winkler, Thomas H., Wirz, Oliver F., Wong, Alicia, Wurst, Peter, Yang, Jennie H. M., Yang, Juhao, Yazdanbakhsh, Maria, Yu, Liping, Yue, Alice, Zhang, Hanlin, Zhao, Yi, Ziegler, Susanne Maria, Zielinski, Christina, Zimmermann, Jakob, and Zychlinsky, Arturo

Abstract

These guidelines are a consensus work of a considerable number of members of the immunology and flow cytometry community. They provide the theory and key practical aspects of flow cytometry enabling immunologists to avoid the common errors that often undermine immunological data. Notably, there are comprehensive sections of all major immune cell types with helpful Tables detailing phenotypes in murine and human cells. The latest flow cytometry techniques and applications are also described, featuring examples of the data that can be generated and, importantly, how the data can be analysed. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid, all written and peer-reviewed by leading experts in the field, making this an essential research companion.

Published
2019

100. Attention to Emotional Information Is Associated With Cytokine Responses to Psychological Stress

Author

Maydych, Viktoriya, Claus, Maren, Watzl, Carsten, and Kleinsorge, Thomas

Subjects
saliva, inflammation, emotional information, psychological stress, attention networks, cytokines, lcsh:Neurosciences. Biological psychiatry. Neuropsychiatry, lcsh:RC321-571, Neuroscience, Original Research
Abstract

This study aimed to investigate the impact of mental stress on salivary cytokines and attention to emotional stimuli, as well as associations between stress-induced changes of immune and cognitive parameters. In a randomized order a total of 60 young adults were assigned to one of two stress conditions with varying stress intensity. High stress was induced by a socially evaluated Paced Auditory Serial Addition Test (PASAT). As a low stress task a paper-and-pencil version of PASAT was administered. Salivary cytokines were measured before, 5 min after, and 45 min after completion of the stress task, and were assayed for pro- and anti-inflammatory cytokines. Three distinct types of attention – alerting, orienting, and executive control – were measured by the modified Emotional Attention Network Test Integration (E-ANTI). IL-1β and IL-6 increased only in the high-stress group. Significant increases in IFN-α, IFN-γ, TNF-α, and IL-10 at 45 min after stress induction (all p’s < 0.05) were observed in both the high-stress and the low-stress group. Alerting attention was positively related to more pronounced increases in IFN-α and TNF-α in both groups. Further, better orienting attention after presentation of negative cues was associated with higher increases in IFN-α, TNF-α, IL-2, IL-5, and IL-10 in both groups, and higher overall levels of IFN-α, IFN-γ, and IL-12p70 in the high-stress group. There were no systematic gender differences in cytokine responses. We conclude that attention processes modulate the increases of salivary cytokines after stress exposure, and that these effects depend on stress level, particular attention network, and stimulus valence.

Published
2018

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