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  1. Article ; Online: Lipid-binding antiphospholipid antibodies: significance for pathophysiology and diagnosis of the antiphospholipid syndrome.

    Müller-Calleja, Nadine / Ruf, Wolfram / Lackner, Karl J

    Critical reviews in clinical laboratory sciences

    2024  , Page(s) 1–18

    Abstract: The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of pathogenic antiphospholipid antibodies (aPL). Since approximately 30 years ago, lipid-binding aPL, which do not require a protein cofactor, have been regarded ... ...

    Abstract The antiphospholipid syndrome (APS) is an autoimmune disease characterized by the presence of pathogenic antiphospholipid antibodies (aPL). Since approximately 30 years ago, lipid-binding aPL, which do not require a protein cofactor, have been regarded as irrelevant for APS pathogenesis even though anticardiolipin are a diagnostic criterion of APS. In this review, we will summarize the available evidence from
    Language English
    Publishing date 2024-01-31
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 280641-1
    ISSN 1549-781X ; 1040-8363 ; 0590-8191
    ISSN (online) 1549-781X
    ISSN 1040-8363 ; 0590-8191
    DOI 10.1080/10408363.2024.2305121
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Rapid translocation of intracellular toll-like receptors depends on endosomal NADPH oxidase.

    Müller-Calleja, Nadine / Hollerbach, Anne / Canisius, Antje / Orning, Carolin / Strand, Susanne / Lackner, Karl J

    European journal of immunology

    2023  Volume 53, Issue 9, Page(s) e2250271

    Abstract: Endosomal toll-like receptors (TLRs) must be translocated from the endoplasmic reticulum (ER) to the endosome and proteolytically cleaved within the endosome before they can induce cellular signals. As ligands for these TLRs are also liberated from ... ...

    Abstract Endosomal toll-like receptors (TLRs) must be translocated from the endoplasmic reticulum (ER) to the endosome and proteolytically cleaved within the endosome before they can induce cellular signals. As ligands for these TLRs are also liberated from apoptotic or necrotic cells, this process is controlled by several mechanisms which shall ensure that there is no inadvertent activation. We have shown previously that antiphospholipid antibodies induce endosomal NADPH-oxidase (NOX) followed by the translocation of TLR7/8 to the endosome. We show now that endosomal NOX is required for the rapid translocation of TLR3, TLR7/8, and TLR9. Deficiency of gp91phox, the catalytic subunit of NOX2, or inhibition of endosomal NOX by the chloride channel blocker niflumic acid both prevent immediate (i.e., within 30 min) translocation of these TLRs as shown by confocal laser scanning microscopy. Under these conditions, the induction of mRNA synthesis for TNF-α and secretion of TNF-α is delayed by approx. 6-9 h. However, maximal expression of TNF-α mRNA or secretion of TNF-α is not significantly reduced. In conclusion, these data add NOX2 as another component involved in the orchestration of cellular responses to ligands of endosomal TLRs.
    MeSH term(s) NADPH Oxidases/metabolism ; Tumor Necrosis Factor-alpha/metabolism ; Toll-Like Receptor 7/genetics ; Ligands ; Toll-Like Receptors/metabolism ; Endosomes ; RNA, Messenger/genetics
    Chemical Substances NADPH Oxidases (EC 1.6.3.-) ; Tumor Necrosis Factor-alpha ; Toll-Like Receptor 7 ; Ligands ; Toll-Like Receptors ; RNA, Messenger
    Language English
    Publishing date 2023-06-27
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 120108-6
    ISSN 1521-4141 ; 0014-2980
    ISSN (online) 1521-4141
    ISSN 0014-2980
    DOI 10.1002/eji.202250271
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  3. Article ; Online: Cofactor-Independent Antiphospholipid Antibodies: Implications for Pathogenesis, Diagnosis, and Treatment of Antiphospholipid Syndrome.

    Lackner, Karl J / Müller-Calleja, Nadine

    Hamostaseologie

    2018  Volume 39, Issue 2, Page(s) 188–194

    Abstract: The antiphospholipid syndrome (APS) has occupied haemostaseologists, rheumatologists and obstetricians since its initial description 35 years ago. Its name has been coined because of the antibodies against phospholipids which were the common property of ... ...

    Abstract The antiphospholipid syndrome (APS) has occupied haemostaseologists, rheumatologists and obstetricians since its initial description 35 years ago. Its name has been coined because of the antibodies against phospholipids which were the common property of affected patients. In particular, the pathogenesis of APS has been intensively studied after the early discovery that it was possible to induce the clinical manifestations in animals by transfer of antiphospholipid antibodies (aPL). In recent years, it has become clear that aPL are not only structurally heterogeneous but also have different pathogenic properties. This review will focus on the relevance of antigenic specificity of aPL in terms of pathogenesis, diagnosis, and perhaps treatment of APS.
    MeSH term(s) Animals ; Antibodies, Antiphospholipid/immunology ; Antiphospholipid Syndrome/diagnosis ; Antiphospholipid Syndrome/etiology ; Antiphospholipid Syndrome/immunology ; Antiphospholipid Syndrome/therapy ; Humans
    Chemical Substances Antibodies, Antiphospholipid
    Language English
    Publishing date 2018-11-12
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 801512-0
    ISSN 2567-5761 ; 0720-9355
    ISSN (online) 2567-5761
    ISSN 0720-9355
    DOI 10.1055/s-0038-1675355
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Response to: 'Protective effects of antimalarials in Chinese patients with systemic lupus erythematosus' by Wang

    Müller-Calleja, Nadine / Lackner, Karl J

    Annals of the rheumatic diseases

    2018  Volume 78, Issue 8, Page(s) e81

    MeSH term(s) Antibodies, Antiphospholipid ; Antimalarials ; Humans ; Hydroxychloroquine ; Lupus Erythematosus, Systemic ; NADPH Oxidases
    Chemical Substances Antibodies, Antiphospholipid ; Antimalarials ; Hydroxychloroquine (4QWG6N8QKH) ; NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2018-06-26
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 7090-7
    ISSN 1468-2060 ; 0003-4967
    ISSN (online) 1468-2060
    ISSN 0003-4967
    DOI 10.1136/annrheumdis-2018-213853
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Diagnosis and Management of the Antiphospholipid Syndrome.

    Lackner, Karl J / Müller‑Calleja, Nadine

    The New England journal of medicine

    2018  Volume 379, Issue 13, Page(s) 1290

    MeSH term(s) Antibodies, Antiphospholipid ; Antiphospholipid Syndrome ; Humans
    Chemical Substances Antibodies, Antiphospholipid
    Language English
    Publishing date 2018-09-10
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 207154-x
    ISSN 1533-4406 ; 0028-4793
    ISSN (online) 1533-4406
    ISSN 0028-4793
    DOI 10.1056/NEJMc1808253
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Pathogenesis of antiphospholipid syndrome: recent insights and emerging concepts.

    Lackner, Karl J / Müller-Calleja, Nadine

    Expert review of clinical immunology

    2018  Volume 15, Issue 2, Page(s) 199–209

    Abstract: ... ...

    Abstract Introduction
    MeSH term(s) Antibodies, Antiphospholipid/genetics ; Antibodies, Antiphospholipid/immunology ; Antiphospholipid Syndrome/genetics ; Antiphospholipid Syndrome/immunology ; Antiphospholipid Syndrome/pathology ; Antiphospholipid Syndrome/therapy ; Blood Coagulation/immunology ; Complement Activation/immunology ; Extracellular Traps/immunology ; Extracellular Vesicles/immunology ; Genetic Heterogeneity ; Humans ; MicroRNAs/immunology ; Neutrophils/immunology
    Chemical Substances Antibodies, Antiphospholipid ; MicroRNAs
    Language English
    Publishing date 2018-12-06
    Publishing country England
    Document type Journal Article ; Review
    ZDB-ID 2274260-8
    ISSN 1744-8409 ; 1744-666X
    ISSN (online) 1744-8409
    ISSN 1744-666X
    DOI 10.1080/1744666X.2019.1546578
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  7. Article ; Online: Endosomal Redox Signaling in the Antiphospholipid Syndrome.

    Lackner, Karl J / Manukyan, Davit / Müller-Calleja, Nadine

    Current rheumatology reports

    2017  Volume 19, Issue 4, Page(s) 20

    Abstract: Purpose of review: It is well established that the antiphospholipid syndrome (APS) is caused by antiphospholipid antibodies (aPL). While several underlying mechanisms have been described in the past, many open questions remain. Here, we will review data ...

    Abstract Purpose of review: It is well established that the antiphospholipid syndrome (APS) is caused by antiphospholipid antibodies (aPL). While several underlying mechanisms have been described in the past, many open questions remain. Here, we will review data on endosomal signaling and, in particular, redox signaling in APS.
    Recent findings: Endosomal redox signaling has been implicated in several cellular processes including signaling of proinflammatory cytokines. We have shown that certain aPL can activate endosomal NADPH-oxidase (NOX) in several cell types followed by induction of proinflammatory and procoagulant cellular responses in vitro. Involvement of endosomes in aPL signaling has also been reported by others. In wild-type mice but not in NOX-deficient mice, aPL accelerate venous thrombus formation underscoring the relevance of endosomal NOX. Furthermore, hydroxychloroquine (HCQ) inhibits activation of endosomal NOX and prevents thrombus formation in aPL-treated mice. Endosomal redox signaling is an important novel mechanism involved in APS pathogenesis. This makes endosomes a potential target for future treatment approaches of APS.
    MeSH term(s) Animals ; Antiphospholipid Syndrome/drug therapy ; Antiphospholipid Syndrome/metabolism ; Endosomes/physiology ; Evidence-Based Medicine/methods ; Humans ; Mice ; NADPH Oxidases/metabolism ; Oxidation-Reduction ; Signal Transduction/physiology ; Venous Thrombosis/metabolism
    Chemical Substances NADPH Oxidases (EC 1.6.3.-)
    Language English
    Publishing date 2017-04
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2057357-1
    ISSN 1534-6307 ; 1523-3774
    ISSN (online) 1534-6307
    ISSN 1523-3774
    DOI 10.1007/s11926-017-0647-7
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Mechanisms of Cellular Activation in the Antiphospholipid Syndrome.

    Müller-Calleja, Nadine / Lackner, Karl J

    Seminars in thrombosis and hemostasis

    2017  Volume 44, Issue 5, Page(s) 483–492

    Abstract: It is long known that antiphospholipid antibodies (aPL) induce proinflammatory and procoagulant cellular responses. The underlying signal transduction has been a major focus of research and is the topic of this review. An amazingly heterogeneous panel of ...

    Abstract It is long known that antiphospholipid antibodies (aPL) induce proinflammatory and procoagulant cellular responses. The underlying signal transduction has been a major focus of research and is the topic of this review. An amazingly heterogeneous panel of signaling pathways has been described and it turns out that at least some of this heterogeneity can be explained by effects of distinct aPL species. On the one hand, there are antibodies against β2-glycoprotein I (β2GPI) which appear to exert their cellular effects only as a complex of β2GPI/anti-β2GPI. Their major targets are low-density lipoprotein-receptor related protein 8 (LRP8), annexin A2 (ANXA2), toll-like receptor 4 (TLR4), and possibly TLR2. The other relevant aPL species are antibodies against cardiolipin which are internalized into endosomes and induce cellular responses via activation of endosomal NADPH-oxidase. Their cell surface target is still unknown. Another important issue relates to the role of complement. It has been shown in vivo that certain pathogenic effects of aPL depend on complement activation, but the exact interplay with the signaling pathways described earlier needs to be elucidated. Thus, while there has been tremendous progress over the past decade, many open questions remain to be answered.
    MeSH term(s) Antiphospholipid Syndrome/immunology ; Humans ; Signal Transduction
    Language English
    Publishing date 2017-02-06
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 196901-8
    ISSN 1098-9064 ; 0094-6176
    ISSN (online) 1098-9064
    ISSN 0094-6176
    DOI 10.1055/s-0036-1597290
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Antiphospholipid Antibodies: Their Origin and Development.

    Lackner, Karl J / Müller-Calleja, Nadine

    Antibodies (Basel, Switzerland)

    2016  Volume 5, Issue 2

    Abstract: Antiphospholipid antibodies (aPL) are a hallmark of the antiphospholipid syndrome (APS), which is the most commonly acquired thrombophilia. To date there is consensus that aPL cause the clinical manifestations of this potentially devastating disorder. ... ...

    Abstract Antiphospholipid antibodies (aPL) are a hallmark of the antiphospholipid syndrome (APS), which is the most commonly acquired thrombophilia. To date there is consensus that aPL cause the clinical manifestations of this potentially devastating disorder. However, there is good evidence that not all aPL are pathogenic. For instance, aPL associated with syphilis show no association with the manifestations of APS. While there has been intensive research on the pathogenetic role of aPL, comparably little is known about the origin and development of aPL. This review will summarize the current knowledge and understanding of the origin and development of aPL derived from animal and human studies.
    Language English
    Publishing date 2016-06-02
    Publishing country Switzerland
    Document type Journal Article ; Review
    ISSN 2073-4468
    ISSN (online) 2073-4468
    DOI 10.3390/antib5020015
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Pathophysiological insights into the antiphospholipid syndrome.

    Lackner, Karl J / Manukyan, Davit / Müller-Calleja, Nadine

    Hamostaseologie

    2016  Volume 37, Issue 3, Page(s) 202–207

    Abstract: The antiphospholipid syndrome (APS) is characterized by venous and/or arterial thrombosis and severe pregnancy morbidity in presence of antiphospholipid antibodies (aPL). While there is compelling evidence that aPL cause the clinical manifestations of ... ...

    Abstract The antiphospholipid syndrome (APS) is characterized by venous and/or arterial thrombosis and severe pregnancy morbidity in presence of antiphospholipid antibodies (aPL). While there is compelling evidence that aPL cause the clinical manifestations of APS, the underlying mechanisms are still a matter of scientific debate. This is mainly related to the broad heterogeneity of aPL. There are three major types of aPL: The first one binds to (anionic) phospholipids, e.g. cardiolipin, in absence of other factors (cofactor independent aPL). The second type binds to phospholipids only in presence of protein cofactors, e.g. ß2-glycoprotein I (ß2GPI) (cofactor dependent aPL). The third type binds to cofactor proteins directly without need for phospholipids. It is widely believed that cofactor independent aPL (type 1) are associated with infections and, more importantly, non-pathogenic, while pathogenic aPL belong to the second and in particular to the third type. This view, in particular with regard to type 1 aPL, has not been undisputed and novel research data have shown that it is in fact untenable. We summarize the available data on the pathogenetic role of aPL and the implications for diagnosis of APS and future research.
    MeSH term(s) Antibodies, Antiphospholipid/blood ; Antiphospholipid Syndrome/diagnosis ; Female ; Humans ; Infection/blood ; Infection/diagnosis ; Pregnancy ; Pregnancy Complications, Hematologic/diagnosis ; Risk Factors ; Thrombosis/diagnosis ; beta 2-Glycoprotein I/blood
    Chemical Substances Antibodies, Antiphospholipid ; beta 2-Glycoprotein I
    Language English
    Publishing date 2016-10-27
    Publishing country Germany
    Document type Journal Article ; Review
    ZDB-ID 801512-0
    ISSN 2567-5761 ; 0720-9355
    ISSN (online) 2567-5761
    ISSN 0720-9355
    DOI 10.5482/HAMO-16-07-0020
    Database MEDical Literature Analysis and Retrieval System OnLINE

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