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Article ; Online: T-cell dysregulation in COVID-19.

Kalfaoglu, Bahire / Almeida-Santos, José / Tye, Chanidapa Adele / Satou, Yorifumi / Ono, Masahiro

Biochemical and biophysical research communications

2020 Volume 538, Page(s) 204–210

Abstract: T-cells play key roles in immunity to COVID-19 as well as the development of severe disease. T-cell immunity to COVID-19 is mediated through differentiated ... ...

Abstract	T-cells play key roles in immunity to COVID-19 as well as the development of severe disease. T-cell immunity to COVID-19 is mediated through differentiated CD4
MeSH term(s)	CD4-Positive T-Lymphocytes/immunology ; COVID-19/immunology ; COVID-19/pathology ; Cytokines/metabolism ; Forkhead Transcription Factors/metabolism ; Humans ; Lymphocyte Activation ; SARS-CoV-2/immunology ; T-Lymphocytes, Cytotoxic/immunology
Chemical Substances	Cytokines ; FOXP3 protein, human ; Forkhead Transcription Factors
Keywords	covid19
Language	English
Publishing date	2020-11-07
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	205723-2
ISSN	1090-2104 ; 0006-291X ; 0006-291X
ISSN (online)	1090-2104 ; 0006-291X
ISSN	0006-291X
DOI	10.1016/j.bbrc.2020.10.079
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Article ; Online: T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis.

Kalfaoglu, Bahire / Almeida-Santos, José / Tye, Chanidapa Adele / Satou, Yorifumi / Ono, Masahiro

Frontiers in immunology

2020 Volume 11, Page(s) 589380

Abstract: Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can ... ...

Abstract	Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19. By
MeSH term(s)	COVID-19/immunology ; COVID-19/virology ; Databases, Genetic ; Forkhead Transcription Factors/metabolism ; Furin/metabolism ; Humans ; Interleukin-2 Receptor alpha Subunit/metabolism ; Lymphocyte Activation/immunology ; Paralysis/immunology ; RNA-Seq ; Receptors, Antigen, T-Cell/metabolism ; SARS-CoV-2/immunology ; Severity of Illness Index ; Single-Cell Analysis/methods ; T-Lymphocytes, Regulatory/immunology ; Transcriptome ; Virus Internalization
Chemical Substances	FOXP3 protein, human ; Forkhead Transcription Factors ; IL2RA protein, human ; Interleukin-2 Receptor alpha Subunit ; Receptors, Antigen, T-Cell ; FURIN protein, human (EC 3.4.21.75) ; Furin (EC 3.4.21.75)
Keywords	covid19
Language	English
Publishing date	2020-10-08
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.589380
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis

Bahire Kalfaoglu / José Almeida-Santos / Chanidapa Adele Tye / Yorifumi Satou / Masahiro Ono

Frontiers in Immunology, Vol

2020 Volume 11

Abstract	Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of FOXP3. Furthermore, we show that CD25+ hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD25-expressing hyperactivated T-cells produce the protease Furin, which facilitates the viral entry of SARS-CoV-2. Collectively, CD4+ T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, which may promote immunopathology. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives immunopathology in severe COVID-19.
Keywords	T-cells ; CD25 ; FOXP3 ; regulatory T-cells (Tregs) ; single cell RNA-seq ; Furin ; Immunologic diseases. Allergy ; RC581-607 ; covid19
Subject code	610 ; 570
Language	English
Publishing date	2020-10-01T00:00:00Z
Publisher	Frontiers Media S.A.
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Audio / Video ; Online: Image_1_T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis.jpg

Bahire Kalfaoglu / José Almeida-Santos / Chanidapa Adele Tye / Yorifumi Satou / Masahiro Ono

2020

Abstract	Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of FOXP3. Furthermore, we show that CD25 + hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD25-expressing hyperactivated T-cells produce the protease Furin, which facilitates the viral entry of SARS-CoV-2. Collectively, CD4 + T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, which may promote immunopathology. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives immunopathology in severe COVID-19.
Keywords	Immunology ; Applied Immunology (incl. Antibody Engineering ; Xenotransplantation and T-cell Therapies) ; Autoimmunity ; Cellular Immunology ; Humoural Immunology and Immunochemistry ; Immunogenetics (incl. Genetic Immunology) ; Innate Immunity ; Transplantation Immunology ; Tumour Immunology ; Immunology not elsewhere classified ; Genetic Immunology ; Animal Immunology ; Veterinary Immunology ; T-cells ; CD25 ; FOXP3 ; regulatory T-cells (Tregs) ; single cell RNA-seq ; Furin ; COVID-19 ; SARS-CoV-2 ; covid19
Subject code	570 ; 610
Publishing date	2020-10-16T05:30:50Z
Publishing country	uk
Document type	Audio / Video ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Audio / Video ; Online: Image_1_T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis.jpg

Bahire Kalfaoglu / José Almeida-Santos / Chanidapa Adele Tye / Yorifumi Satou / Masahiro Ono

2020

Abstract	Severe COVID-19 patients show various immunological abnormalities including T-cell reduction and cytokine release syndrome, which can be fatal and is a major concern of the pandemic. However, it is poorly understood how T-cell dysregulation can contribute to the pathogenesis of severe COVID-19. Here we show single cell-level mechanisms for T-cell dysregulation in severe COVID-19, demonstrating new pathogenetic mechanisms of T-cell activation and differentiation underlying severe COVID-19. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of FOXP3. Furthermore, we show that CD25 + hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD25-expressing hyperactivated T-cells produce the protease Furin, which facilitates the viral entry of SARS-CoV-2. Collectively, CD4 + T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, which may promote immunopathology. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives immunopathology in severe COVID-19.
Keywords	Immunology ; Applied Immunology (incl. Antibody Engineering ; Xenotransplantation and T-cell Therapies) ; Autoimmunity ; Cellular Immunology ; Humoural Immunology and Immunochemistry ; Immunogenetics (incl. Genetic Immunology) ; Innate Immunity ; Transplantation Immunology ; Tumour Immunology ; Immunology not elsewhere classified ; Genetic Immunology ; Animal Immunology ; Veterinary Immunology ; T-cells ; CD25 ; FOXP3 ; regulatory T-cells (Tregs) ; single cell RNA-seq ; Furin ; COVID-19 ; SARS-CoV-2 ; covid19
Subject code	570 ; 610
Publishing date	2020-10-08T04:57:11Z
Publishing country	uk
Document type	Audio / Video ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: T-Cell Hyperactivation and Paralysis in Severe COVID-19 Infection Revealed by Single-Cell Analysis

Kalfaoglu, Bahire / Almeida-Santos, José / Tye, Chanidapa Adele / Satou, Yorifumi / Ono, Masahiro

Frontiers in Immunology

2020 Volume 11

Keywords	covid19
Publisher	Frontiers Media SA
Publishing country	ch
Document type	Article ; Online
ZDB-ID	2606827-8
ISSN	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2020.589380
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: T-cell dysregulation in COVID-19

Kalfaoglu, Bahire / Almeida-Santos, José / Tye, Chanidapa Adele / Satou, Yorifumi / Ono, Masahiro

Biochemical and Biophysical Research Communications ; ISSN 0006-291X

2020

Keywords	Biophysics ; Cell Biology ; Biochemistry ; Molecular Biology ; covid19
Language	English
Publisher	Elsevier BV
Publishing country	us
Document type	Article ; Online
DOI	10.1016/j.bbrc.2020.10.079
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Temporal profiling of CD4 T-cell activation and differentiation upon SARS-CoV-2 spike protein immunisation

Almeida-Santos, José / Berkachy, Rita / Tye, Chanidapa Adele / Hassan, Jehanne / Kalfaoglu, Bahire / Selkirk, Murray E / Ono, Masahiro

bioRxiv

Abstract: CD4 T-cells require T-cell receptor (TCR) signalling for their activation and differentiation. Foxp3+ regulatory T-cells (Treg) are dependent on TCR signals for their differentiation and suppressive function. However, it is not fully known how TCR ... ...

Abstract	CD4 T-cells require T-cell receptor (TCR) signalling for their activation and differentiation. Foxp3+ regulatory T-cells (Treg) are dependent on TCR signals for their differentiation and suppressive function. However, it is not fully known how TCR signalling controls the differentiation of polyclonal CD4 T-cells upon antigen recognition at the single-cell level in vivo. In this study, using Nr4a3-Tocky (Timer-of-cell-kinetics-and-activity), which analyses temporal changes of antigen-reactive T-cells following TCR signalling, we investigated T-cell response to Spike protein fragments (S1a, S1b, S2a, and S2b) upon immunisation. We show that S1a and S2a induced the differentiation of PD1hiCXCR5+ T follicular helper (Tfh) cells, which is related to CD4 T-cell immunogenicity. In contrast, S1b induced CD25hiGITRhiPD-1int Treg, which intermittently received TCR signalling. Using Foxp3-Tocky, which analyses Foxp3 transcriptional dynamics, the S1b-reactive Treg sustained Foxp3 transcription over time, which is a hallmark of activated Treg. Foxp3 fate-mapping showed that the S1b-reactive Treg were derived not from pre-existing thymic Treg, suggesting Foxp3 induction in non-Treg cells. Thus, the current study reveals temporally dynamic differentiation of CD4 T-cells and Treg upon immunisation in the polyclonal TCR repertoire.
Keywords	covid19
Language	English
Publishing date	2022-07-21
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2022.07.21.500987
Database	COVID19

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Article ; Online: T-cell hyperactivation and paralysis in severe COVID-19 infection revealed by single-cell analysis

Kalfaoglu, Bahire / Almeida-Santos, José / Adele Tye, Chanidapa / Satou, Yorifumi / Ono, Masahiro

bioRxiv

Abstract: Severe COVID-19 patients can show respiratory failure, T-cell reduction, and cytokine release syndrome (CRS), which can be fatal in both young and aged patients and is a major concern of the pandemic. However, the pathogenetic mechanisms of CRS in COVID- ... ...

Abstract	Severe COVID-19 patients can show respiratory failure, T-cell reduction, and cytokine release syndrome (CRS), which can be fatal in both young and aged patients and is a major concern of the pandemic. However, the pathogenetic mechanisms of CRS in COVID-19 are poorly understood. Here we show single cell-level mechanisms for T-cell dysregulation in severe SARS-CoV-2 infection, and thereby demonstrate the mechanisms underlying T-cell hyperactivation and paralysis in severe COVID-19 patients. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of the transcription factor FOXP3 and interestingly, both the differentiation of regulatory T-cells (Tregs) and Th17 was inhibited. Meanwhile, highly activated CD4+ T-cells express PD-1 alongside macrophages that express PD-1 ligands in severe patients, suggesting that PD-1-mediated immunoregulation was partially operating. Furthermore, we show that CD25+ hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD4+ T-cells, particularly CD25-expressing hyperactivated T-cells, produce the protease Furin, which facilitates the viral entry of SARS-CoV-2. Collectively, CD4+ T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, while activated CD4+ T-cells continue to promote further viral infection through the production of Furin. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives pulmonary damage, systemic CRS and organ failure in severe COVID-19 patients.
Keywords	covid19
Publisher	BioRxiv; WHO
Document type	Article ; Online
DOI	10.1101/2020.05.26.115923
Database	COVID19

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Article ; Online: T-cell hyperactivation and paralysis in severe COVID-19 infection revealed by single-cell analysis

Kalfaoglu, Bahire / Almeida-Santos, José / Tye, Chanidapa Adele / Satou, Yorifumi / Ono, Masahiro

bioRxiv

Abstract	Severe COVID-19 patients can show respiratory failure, T-cell reduction, and cytokine release syndrome (CRS), which can be fatal in both young and aged patients and is a major concern of the pandemic. However, the pathogenetic mechanisms of CRS in COVID-19 are poorly understood. Here we show single cell-level mechanisms for T-cell dysregulation in severe SARS-CoV-2 infection, and thereby demonstrate the mechanisms underlying T-cell hyperactivation and paralysis in severe COVID-19 patients. By in silico sorting CD4+ T-cells from a single cell RNA-seq dataset, we found that CD4+ T-cells were highly activated and showed unique differentiation pathways in the lung of severe COVID-19 patients. Notably, those T-cells in severe COVID-19 patients highly expressed immunoregulatory receptors and CD25, whilst repressing the expression of the transcription factor FOXP3 and interestingly, both the differentiation of regulatory T-cells (Treg) and Th17 was inhibited. Meanwhile, highly activated CD4+ T-cells express PD-1 alongside macrophages that express PD-1 ligands in severe patients, suggesting that PD-1-mediated immunoregulation was partially operating. Furthermore, we show that CD25+ hyperactivated T-cells differentiate into multiple helper T-cell lineages, showing multifaceted effector T-cells with Th1 and Th2 characteristics. Lastly, we show that CD4+ T-cells, particularly CD25-expressing hyperactivated T-cells, produce the protease Furin, which facilitates the viral entry of SARS- CoV-2. Collectively, CD4+ T-cells from severe COVID-19 patients are hyperactivated and FOXP3-mediated negative feedback mechanisms are impaired in the lung, while activated CD4+ T-cells continue to promote further viral infection through the production of Furin. Therefore, our study proposes a new model of T-cell hyperactivation and paralysis that drives pulmonary damage, systemic CRS and organ failure in severe COVID-19 patients.
Keywords	covid19
Language	English
Publishing date	2020-05-26
Publisher	Cold Spring Harbor Laboratory
Document type	Article ; Online
DOI	10.1101/2020.05.26.115923
Database	COVID19

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