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  1. Book ; Online: Arrest chemokines

    Ley, Klaus

    2015  

    Abstract: Arrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T ... ...

    Abstract Arrest chemokines are a small group of chemokines that promote leukocyte arrest from rolling by triggering rapid integrin activation. Arrest chemokines have been described for neutrophils, monocytes, eosinophils, naïve lymphocytes and effector memory T cells. Most arrest chemokines are immobilized on the endothelial surface by binding to heparin sulfate proteoglycans. Whether soluble chemokines can promote integrin activation and arrest is controversial (Alon-Gerszten). Many aspects of the signaling pathway from the GPCR chemokine receptor to integrin activation are the subject of active investigation. Leukocyte adhesion deficiency III is a human disease in which chemokine-triggered integrin activation is defective because of a mutation in the cytoskeletal protein kindlin-3. About 10 different such mutations have been described. The defects seen in patients with LAD-III elucidate the importance of rapid integrin activation for host defense in humans. We welcome reports that help clarifying this crucial first step in the process of leukocyte transendothelial migration
    Keywords Immunologic diseases. Allergy ; Medicine (General)
    Size 1 electronic resource (108 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020090521
    ISBN 9782889194308 ; 2889194302
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  2. Article ; Online: Neutrophil ion currents matter.

    Ley, Klaus

    Cardiovascular research

    2022  Volume 118, Issue 5, Page(s) 1165–1166

    MeSH term(s) Neutrophils
    Language English
    Publishing date 2022-03-03
    Publishing country England
    Document type Editorial ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvac025
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 565: Show issues Location:
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  3. Book: Adhesion molecules

    Ley, Klaus

    function and inhibition

    (Progress in inflammation research)

    2007  

    Author's details Klaus Ley, ed
    Series title Progress in inflammation research
    Keywords Leukozytenadhäsion ; Zell-Adhäsionsmolekül
    Subject CAM ; Cell adhesion molecule ; Zelladhäsionsmolekül ; Adhäsions-Molekül
    Subject code 612.112
    Language English
    Size XIV, 309 S. : Ill., graph. Darst., 24 cm
    Publisher Birkhäuser
    Publishing place Basel u.a.
    Publishing country Switzerland ; Germany ; United States
    Document type Book
    Note Literaturangaben
    HBZ-ID HT015560098
    ISBN 978-3-7643-7974-2 ; 3-7643-7974-X ; 9783764379759 ; 3764379758
    Database Catalogue ZB MED Medicine, Health

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    Shelf markLoan statusLocation
    2008 A 3835 order for loan Magazin

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  4. Article ; Online: Immunotherapy for atherosclerosis by targeting pro-inflammatory T cells.

    Khan, Amir / Ley, Klaus

    Cell research

    2024  

    Language English
    Publishing date 2024-04-02
    Publishing country England
    Document type Journal Article
    ZDB-ID 1319303-x
    ISSN 1748-7838 ; 1001-0602
    ISSN (online) 1748-7838
    ISSN 1001-0602
    DOI 10.1038/s41422-024-00955-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Inflammation and Atherosclerosis.

    Ley, Klaus

    Cells

    2021  Volume 10, Issue 5

    Abstract: This 11-chapter Special Issue ... ...

    Abstract This 11-chapter Special Issue of
    MeSH term(s) Animals ; Atherosclerosis/immunology ; Disease Models, Animal ; Humans ; Inflammation/immunology ; Translational Medical Research/methods
    Language English
    Publishing date 2021-05-14
    Publishing country Switzerland
    Document type Editorial
    ZDB-ID 2661518-6
    ISSN 2073-4409 ; 2073-4409
    ISSN (online) 2073-4409
    ISSN 2073-4409
    DOI 10.3390/cells10051197
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Fortified Tregs to fight atherosclerosis.

    Ley, Klaus

    Cardiovascular research

    2021  Volume 117, Issue 9, Page(s) 1987–1988

    MeSH term(s) Atherosclerosis/prevention & control ; Humans ; Plaque, Atherosclerotic
    Language English
    Publishing date 2021-03-17
    Publishing country England
    Document type Editorial ; Research Support, N.I.H., Extramural ; Comment
    ZDB-ID 80340-6
    ISSN 1755-3245 ; 0008-6363
    ISSN (online) 1755-3245
    ISSN 0008-6363
    DOI 10.1093/cvr/cvab103
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Role of the adaptive immune system in atherosclerosis.

    Ley, Klaus

    Biochemical Society transactions

    2020  Volume 48, Issue 5, Page(s) 2273–2281

    Abstract: Atherosclerosis, the pathology underlying heart attacks, strokes and peripheral artery disease, is a chronic inflammatory disease of the artery wall initiated by elevated low-density lipoprotein (LDL) cholesterol levels. LDL accumulates in the artery ... ...

    Abstract Atherosclerosis, the pathology underlying heart attacks, strokes and peripheral artery disease, is a chronic inflammatory disease of the artery wall initiated by elevated low-density lipoprotein (LDL) cholesterol levels. LDL accumulates in the artery wall, where it can become oxidized to oxLDL. T cell responses to ApoB, a core protein found in LDL and other lipoproteins, are detectable in healthy mice and people. Most of the ApoB-specific CD4T cells are FoxP3+ regulatory T cells (Treg). In the course of atherosclerosis development, the number of ApoB-reactive T cells expands. At the same time, their phenotype changes, showing cell surface markers, transcription factors and transcriptomes resembling other T-helper lineages like Th17, Th1 and follicular helper (TFH) cells. TFH cells enter germinal centers and provide T cell help to B cells, enabling antibody isotype switch from IgM to IgG and supporting affinity maturation. In people and mice with atherosclerosis, IgG and IgM antibodies to oxLDL are detectable. Higher IgM antibody titers to oxLDL are associated with less, IgG antibodies with more atherosclerosis. Thus, both T and B cells play critical roles in atherosclerosis. Modifying the adaptive immune response to ApoB holds promise for preventing atherosclerosis and reducing disease burden.
    MeSH term(s) Adaptive Immunity ; Animals ; Apolipoprotein B-100/metabolism ; Atherosclerosis/immunology ; Atherosclerosis/physiopathology ; Biomarkers ; CD4-Positive T-Lymphocytes/cytology ; Cell Proliferation ; Cholesterol, LDL/chemistry ; Humans ; Immune System ; Immunoglobulin G/immunology ; Inflammation ; Lipoproteins, LDL/chemistry ; Mice ; Oxidation-Reduction ; Risk ; T-Lymphocytes/cytology ; T-Lymphocytes, Helper-Inducer ; T-Lymphocytes, Regulatory/metabolism ; Th17 Cells
    Chemical Substances APOB protein, human ; Apolipoprotein B-100 ; Biomarkers ; Cholesterol, LDL ; Immunoglobulin G ; Lipoproteins, LDL ; oxidized low density lipoprotein
    Language English
    Publishing date 2020-09-01
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 184237-7
    ISSN 1470-8752 ; 0300-5127
    ISSN (online) 1470-8752
    ISSN 0300-5127
    DOI 10.1042/BST20200602
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.A 944: Show issues Location:
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  8. Book ; Online: M1/M2 Macrophages: The Arginine Fork in the Road to Health and Disease

    Lenz, Laurel L / Mills, Charles Dudley / Ley, Klaus

    2015  

    Abstract: Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either Kill ... ...

    Abstract Macrophages have unique and diverse functions necessary for survival. And, in humans (and other species), they are the most abundant leukocytes in tissues. The Innate functions of macrophages that are best known are their unusual ability to either Kill or Repair. Since killing is a destructive process and repair is a constructive process, it was stupefying how one cell could exhibit these 2 polar - opposite functions. However, in the late 1980's, it was shown that macrophages have a unique ability to enzymatically metabolize Arginine to Nitric Oxide (NO, a gaseous non - specific killer molecule) or to Ornithine (a precursor of polyamines and collagen for repair). The dual Arginine metabolic capacity of macrophages provided a functional explanation for their ability to kill or repair. Macrophages predominantly producing NO are called M1 and those producing Ornithine are called M2.-

    M1 and M2 - dominant responses occur in lower vertebrates, and in T cell deficient vertebrates being directly driven by Damage and Pathogen Associated Molecular Patterns (DAMP and PAMP). Thus, M1 and M2 are Innate responses that protect the host without Adaptive Immunity. In turn, M1/M2 is supplanting previous models in which T cells were necessary to activate or alternatively activate macrophages (the Th1/Th2 paradigm). M1 and M2 macrophages were named such because of the additional key findings that these macrophages stimulate Th1 and Th2 - like responses, respectively. So, in addition to their unique ability to kill or repair, macrophages also govern Adaptive Immunity. All of the foregoing would be less important if M1 or M2 - dominant responses were not observed in disease. But, they are. The best example to date is the predominance of M2 macrophages in human tumors where they act like wound repair macrophages and actively promote growth.-

    More generally, humans have become M2 - dominant because sanitation, antibiotics and vaccines have lessened M1 responses. And, M2 dominance seems the cause of ever - increasing allergies in developed countries. Obesity represents a new and different circumstance. Surfeit energy (e.g., lipoproteins) causes monocytes to become M1 dominant in the vessel walls causing plaques. Because M1 or M2 dominant responses are clearly causative in many modern diseases, there is great potential in developing the means to selectively stimulate (or inhibit) either M1 or M2 responses to kill or repair, or to stimulate Th1 or Th2 responses, depending on the circumstance. The contributions here are meant to describe diseases of M1 or M2 dominance, and promising new methodologies to modulate the fungible metabolic machinery of macrophages for better health
    Keywords Immunologic diseases. Allergy ; Medicine (General)
    Size 1 electronic resource (280 p.)
    Publisher Frontiers Media SA
    Document type Book ; Online
    Note English ; Open Access
    HBZ-ID HT020090106
    ISBN 9782889194995 ; 288919499X
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  9. Book: Physiology of inflammation

    Ley, Klaus

    (The American Physiological Society methods in physiology series ; 3)

    2001  

    Author's details ed. by Klaus Ley
    Series title The American Physiological Society methods in physiology series ; 3
    Collection
    Keywords Inflammation / immunology ; Inflammation / physiopathology ; Inflammation Mediators
    Language English
    Size XII, 546 S. : Ill., graph. Darst.
    Publisher Oxford Univ. Press
    Publishing place New York u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT013393928
    ISBN 0-19-512829-X ; 978-0-19-512829-1
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

    Shelf markLoan statusLocation
    2004 A 2860 order for loan Magazin

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  10. Article ; Online: Breaking tolerance: the autoimmune aspect of atherosclerosis.

    Khan, Amir / Roy, Payel / Ley, Klaus

    Nature reviews. Immunology

    2024  

    Abstract: Atherosclerotic cardiovascular disease (ASCVD) is a chronic inflammatory disease of the arterial walls and is characterized by the accumulation of lipoproteins that are insufficiently cleared by phagocytes. Following the initiation of atherosclerosis, ... ...

    Abstract Atherosclerotic cardiovascular disease (ASCVD) is a chronic inflammatory disease of the arterial walls and is characterized by the accumulation of lipoproteins that are insufficiently cleared by phagocytes. Following the initiation of atherosclerosis, the pathological progression is accelerated by engagement of the adaptive immune system. Atherosclerosis triggers the breakdown of tolerance to self-components. This loss of tolerance is reflected in defective expression of immune checkpoint molecules, dysfunctional antigen presentation, and aberrations in T cell populations - most notably in regulatory T (T
    Language English
    Publishing date 2024-03-12
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2062776-2
    ISSN 1474-1741 ; 1474-1733
    ISSN (online) 1474-1741
    ISSN 1474-1733
    DOI 10.1038/s41577-024-01010-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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