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  1. Article ; Online: Asthma: From Diagnosis to Endotype to Treatment.

    Lodge, Katharine M / Knolle, Martin D / Jha, Akhilesh

    American journal of respiratory and critical care medicine

    2018  Volume 197, Issue 8, Page(s) 1065–1067

    MeSH term(s) Antibodies, Monoclonal, Humanized ; Asthma ; Glucocorticoids ; Humans ; Phenotype
    Chemical Substances Antibodies, Monoclonal, Humanized ; Glucocorticoids ; benralizumab (71492GE1FX)
    Language English
    Publishing date 2018-05-03
    Publishing country United States
    Document type Journal Article ; Comment
    ZDB-ID 1180953-x
    ISSN 1535-4970 ; 0003-0805 ; 1073-449X
    ISSN (online) 1535-4970
    ISSN 0003-0805 ; 1073-449X
    DOI 10.1164/rccm.201710-2139RR
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Uh II Zs.80: Show issues Location:
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  2. Article ; Online: An αvβ3 integrin checkpoint is critical for efficient T

    Szeto, Aydan C H / Ferreira, Ana C F / Mannion, Jonathan / Clark, Paula A / Sivasubramaniam, Meera / Heycock, Morgan W D / Crisp, Alastair / Jolin, Helen E / Kozik, Patrycja / Knolle, Martin D / McKenzie, Andrew N J

    Nature immunology

    2022  Volume 24, Issue 1, Page(s) 123–135

    Abstract: ... Naive ... ...

    Abstract Naive CD4
    MeSH term(s) Mice ; Animals ; Cytokines/metabolism ; Th2 Cells ; Cell Differentiation ; Allergens ; Lung ; Mammals/metabolism
    Chemical Substances Cytokines ; Allergens
    Language English
    Publishing date 2022-12-22
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/s41590-022-01378-w
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 42: Show issues

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  3. Book: D. Martin Luthers letzte Tage im Zeugnis seiner letzten Briefe, Tischreden, Predigten, Schriften und seiner Freunde

    Knolle, Theodor / Luther, Martin

    1946  

    Author's details zsgest. von Theodor Knolle
    Language German
    Size 48 S
    Publisher Nölke
    Publishing place Hamburg
    Document type Book
    Note In Fraktur
    Database Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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  4. Article ; Online: Asthma, ECMO and eosinophils.

    McLellan, Tom / Patvardhan, Chinmay / Rassl, Doris / Jenkins, Huw Steven / Knolle, Martin / Thillai, Muhunthan

    Thorax

    2021  Volume 76, Issue 7, Page(s) 737–739

    MeSH term(s) Adult ; Asthma/diagnosis ; Asthma/metabolism ; Asthma/therapy ; Eosinophils/pathology ; Extracorporeal Membrane Oxygenation/methods ; Humans ; Leukocyte Count ; Male
    Language English
    Publishing date 2021-01-25
    Publishing country England
    Document type Case Reports ; Journal Article
    ZDB-ID 204353-1
    ISSN 1468-3296 ; 0040-6376
    ISSN (online) 1468-3296
    ISSN 0040-6376
    DOI 10.1136/thoraxjnl-2020-216052
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Prolonged norovirus infections correlate to quasispecies evolution resulting in structural changes of surface-exposed epitopes.

    Afridi, Suliman Qadir / Usman, Zainab / Donakonda, Sainitin / Wettengel, Jochen Martin / Velkov, Stoyan / Beck, Robert / Gerhard, Markus / Knolle, Percy / Frishman, Dmitrij / Protzer, Ulrike / Moeini, Hassan / Hoffmann, Dieter

    iScience

    2021  Volume 24, Issue 7, Page(s) 102802

    Abstract: ... antigenic epitopes A, D, and E. The number of quasispecies increased in infections lasting for >1 month ...

    Abstract In this study, we analyzed norovirus (NoV) evolution in sequential samples of six chronically infected patients. The capsid gene was amplified from stool samples, and deep sequencing was performed. The role of amino acid flexibility in structural changes and ligand binding was studied with molecular dynamics (MD) simulations. Concentrations of capsid-specific antibodies increased in sequential sera. Capsid sequences accumulated mutations during chronic infection, particularly in the surface-exposed antigenic epitopes A, D, and E. The number of quasispecies increased in infections lasting for >1 month. Interestingly, high genetic complexity and distances were followed by ongoing NoV replication, whereas lower genetic complexity and distances preceded cure. MD simulation revealed that surface-exposed amino acid substitutions of the P2 domain caused fluctuation of blockade epitopes. In conclusion, the capsid protein accumulates numerous mutations during chronic infection; however, only those on the protein surface change the protein structure substantially and may lead to immune escape.
    Language English
    Publishing date 2021-06-30
    Publishing country United States
    Document type Journal Article
    ISSN 2589-0042
    ISSN (online) 2589-0042
    DOI 10.1016/j.isci.2021.102802
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Combining clinical, radiological and genetic approaches to pneumothorax management.

    Grimes, Hannah L / Holden, Simon / Babar, Judith / Karia, Sumit / Wetscherek, Maria Ta / Barker, Allanah / Herre, Jurgen / Knolle, Martin D / Maher, Eamonn R / Marciniak, Stefan John

    Thorax

    2021  Volume 77, Issue 2, Page(s) 196–198

    Abstract: Familial spontaneous pneumothorax (FSP) accounts for 10% of primary spontaneous pneumothoraces. Appropriate investigation of FSP enables early diagnosis of serious monogenic diseases and the practice of precision medicine. Here, we show that a ... ...

    Abstract Familial spontaneous pneumothorax (FSP) accounts for 10% of primary spontaneous pneumothoraces. Appropriate investigation of FSP enables early diagnosis of serious monogenic diseases and the practice of precision medicine. Here, we show that a pneumothorax genetics multidisciplinary team (MDT) can efficiently diagnose a range of syndromic causes of FSP. A sizeable group (73.6%) of clinically unclassifiable FSPs remains. Using whole genome sequencing we demonstrate that most of these cases are not known monogenic disorders. Therefore, clinico-radiological assessment by an MDT has high sensitivity for currently known clinically important monogenic causes of FSP, which has relevance for the design of efficient pneumothorax services.
    MeSH term(s) Humans ; Pneumothorax/diagnostic imaging ; Pneumothorax/genetics ; Pneumothorax/therapy ; Precision Medicine
    Language English
    Publishing date 2021-06-18
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 204353-1
    ISSN 1468-3296 ; 0040-6376
    ISSN (online) 1468-3296
    ISSN 0040-6376
    DOI 10.1136/thoraxjnl-2021-217210
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: IL-25 as a potential therapeutic target in allergic asthma.

    Knolle, Martin D / Rana, Batika M / McKenzie, Andrew N J

    Immunotherapy

    2015  Volume 7, Issue 6, Page(s) 607–610

    MeSH term(s) Asthma/immunology ; Asthma/pathology ; Asthma/therapy ; Humans ; Interleukin-17/antagonists & inhibitors ; Interleukin-17/immunology ; Portraits as Topic
    Chemical Substances IL25 protein, human ; Interleukin-17
    Language English
    Publishing date 2015-06-23
    Publishing country England
    Document type Journal Article
    ZDB-ID 2495964-9
    ISSN 1750-7448 ; 1750-743X
    ISSN (online) 1750-7448
    ISSN 1750-743X
    DOI 10.2217/imt.15.36
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: ADAM8: a new therapeutic target for asthma.

    Knolle, Martin D / Owen, Caroline A

    Expert opinion on therapeutic targets

    2009  Volume 13, Issue 5, Page(s) 523–540

    Abstract: Background: A proteinase with a disintegrin and a metalloproteinase domain-8 (ADAM8) has been linked to asthma.: Objective: To explore whether ADAM8 is a therapeutic target for asthma.: Methods: We reviewed literature on ADAM8's function and ... ...

    Abstract Background: A proteinase with a disintegrin and a metalloproteinase domain-8 (ADAM8) has been linked to asthma.
    Objective: To explore whether ADAM8 is a therapeutic target for asthma.
    Methods: We reviewed literature on ADAM8's function and expression and activities in lungs of humans and mice with allergic airway inflammation (AAI). We used these data to generate hypotheses about the contributions of ADAM8 to asthma pathogenesis.
    Conclusions: ADAM8 levels are increased in airway epithelium and airway inflammatory cells in mice with AAI and human asthma patients. Data from murine models of AAI indicate that ADAM8 dampens airway inflammation. It is not clear whether ADAM8 contributes directly to structural remodeling in asthmatic airways. Additional studies are required to validate ADAM8 as a therapeutic target for asthma.
    MeSH term(s) ADAM Proteins/antagonists & inhibitors ; ADAM Proteins/chemistry ; ADAM Proteins/deficiency ; ADAM Proteins/physiology ; Animals ; Anti-Asthmatic Agents/pharmacology ; Anti-Asthmatic Agents/therapeutic use ; Antigens, CD ; Asthma/drug therapy ; Asthma/enzymology ; Asthma/immunology ; Asthma/pathology ; Child ; Cytokines/metabolism ; Drug Delivery Systems ; Drug Evaluation, Preclinical ; Epithelial Cells/enzymology ; Extracellular Matrix Proteins/metabolism ; Fibrosis ; Humans ; Leukocytes/enzymology ; Lung/enzymology ; Lung/pathology ; Membrane Proteins/antagonists & inhibitors ; Membrane Proteins/chemistry ; Membrane Proteins/deficiency ; Membrane Proteins/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Protease Inhibitors/pharmacology ; Protease Inhibitors/therapeutic use ; Protein Structure, Tertiary ; Pulmonary Eosinophilia/drug therapy ; Pulmonary Eosinophilia/enzymology ; Pulmonary Eosinophilia/etiology ; Receptors, Cell Surface/metabolism
    Chemical Substances Anti-Asthmatic Agents ; Antigens, CD ; Cytokines ; Extracellular Matrix Proteins ; Membrane Proteins ; Protease Inhibitors ; Receptors, Cell Surface ; ADAM Proteins (EC 3.4.24.-) ; ADAM8 protein, human (EC 3.4.24.-) ; Adam8 protein, mouse (EC 3.4.24.-)
    Language English
    Publishing date 2009-06-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2055208-7
    ISSN 1744-7631 ; 1472-8222
    ISSN (online) 1744-7631
    ISSN 1472-8222
    DOI 10.1517/14728220902889788
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 5244: Show issues Location:
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  9. Article ; Online: Enolase represents a metabolic checkpoint controlling the differential exhaustion programmes of hepatitis virus-specific CD8

    Winkler, Frances / Hipp, Anna V / Ramirez, Carlos / Martin, Bianca / Villa, Matteo / Neuwirt, Emilia / Gorka, Oliver / Aerssens, Jeroen / Johansson, Susanne E / Rana, Nisha / Llewellyn-Lacey, Sian / Price, David A / Panning, Marcus / Groß, Olaf / Pearce, Erika L / Hermann, Carl M / Schumann, Kathrin / Hannibal, Luciana / Neumann-Haefelin, Christoph /
    Boettler, Tobias / Knolle, Percy / Hofmann, Maike / Wohlleber, Dirk / Thimme, Robert / Bengsch, Bertram

    Gut

    2023  Volume 72, Issue 10, Page(s) 1971–1984

    Abstract: Objective: Exhausted T cells with limited effector function are enriched in chronic hepatitis B and C virus (HBV and HCV) infection. Metabolic regulation contributes to exhaustion, but it remains unclear how metabolism relates to different exhaustion ... ...

    Abstract Objective: Exhausted T cells with limited effector function are enriched in chronic hepatitis B and C virus (HBV and HCV) infection. Metabolic regulation contributes to exhaustion, but it remains unclear how metabolism relates to different exhaustion states, is impacted by antiviral therapy, and if metabolic checkpoints regulate dysfunction.
    Design: Metabolic state, exhaustion and transcriptome of virus-specific CD8
    Results: HBV-specific (core
    Conclusion: Metabolism of HBV-specific and HCV-specific T cells is strongly connected to their exhaustion severity. Our results highlight enolase as metabolic regulator of severely exhausted T cells. They connect differential bioenergetic fitness with distinct exhaustion subtypes and varying liver disease, with implications for therapeutic strategies.
    MeSH term(s) Humans ; Animals ; Mice ; CD8-Positive T-Lymphocytes/metabolism ; Antiviral Agents/therapeutic use ; Persistent Infection ; Hepatitis C, Chronic/drug therapy ; Hepatitis B, Chronic/drug therapy ; Hepatitis B, Chronic/metabolism ; Hepatitis C/drug therapy ; Hepatitis Viruses ; Hepatitis B virus
    Chemical Substances Antiviral Agents
    Language English
    Publishing date 2023-08-04
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80128-8
    ISSN 1468-3288 ; 0017-5749
    ISSN (online) 1468-3288
    ISSN 0017-5749
    DOI 10.1136/gutjnl-2022-328734
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: MicroRNA-155 Protects Group 2 Innate Lymphoid Cells From Apoptosis to Promote Type-2 Immunity.

    Knolle, Martin D / Chin, Shau Bing / Rana, Batika M J / Englezakis, Alexandros / Nakagawa, Rinako / Fallon, Padraic G / Git, Anna / McKenzie, Andrew N J

    Frontiers in immunology

    2018  Volume 9, Page(s) 2232

    Abstract: Group-2 innate lymphoid cells (ILC2) play critical roles in the initiation and maintenance of type-2 immune responses, predominantly through their production of the type-2 cytokines IL-5, IL-9, and IL-13. ILC2 are essential for the efficient elimination ... ...

    Abstract Group-2 innate lymphoid cells (ILC2) play critical roles in the initiation and maintenance of type-2 immune responses, predominantly through their production of the type-2 cytokines IL-5, IL-9, and IL-13. ILC2 are essential for the efficient elimination of helminth parasites, but also contribute to the detrimental type-2 immune responses that underlie diseases such as asthma and allergy. While several transcription factors have been identified that regulate the development and function of ILC2, less is known about the post-transcriptional mechanisms that regulate these processes. We identified micro-RNAs (miRNAs) that are co-ordinately regulated in ILC2 from mice exposed to two different stimuli, namely IL-33 "alarmin" administration or
    MeSH term(s) Animals ; Apoptosis/genetics ; Apoptosis/immunology ; Cell Survival/genetics ; Cell Survival/immunology ; Cells, Cultured ; Cytokines/genetics ; Cytokines/immunology ; Cytokines/metabolism ; Gene Expression Profiling/methods ; Gene Expression Regulation/immunology ; Immunity, Innate/genetics ; Immunity, Innate/immunology ; Interleukin-33/immunology ; Lymphocytes/immunology ; Lymphocytes/metabolism ; Lymphocytes/parasitology ; Mice, Knockout ; Mice, Transgenic ; MicroRNAs/genetics ; MicroRNAs/immunology ; MicroRNAs/metabolism ; Nippostrongylus/immunology ; Nippostrongylus/physiology ; Th2 Cells/immunology ; Th2 Cells/metabolism ; Th2 Cells/parasitology
    Chemical Substances Cytokines ; Interleukin-33 ; MicroRNAs ; Mirn155 microRNA, mouse
    Language English
    Publishing date 2018-10-09
    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.2018.02232
    Database MEDical Literature Analysis and Retrieval System OnLINE

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