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  1. Book: The molecular pathology of autoimmune diseases

    Theofilopoulos, Argyrios N.

    2002  

    Author's details ed. by Argyrios N. Theofilopoulos
    Keywords Autoimmune Diseases / genetics ; Autoimmune Diseases / pathology ; Autoimmunity ; Autoaggressionskrankheit ; Molekularpathologie
    Subject Autoantikörperkrankheit ; Autoimmunkrankheit ; Autoimmunopathie ; Autoimmunerkrankung
    Language English
    Size XIX, 1191 S. : Ill., graph. Darst.
    Edition 2. ed.
    Publisher Taylor & Francis
    Publishing place New York, NY u.a.
    Publishing country United States
    Document type Book
    HBZ-ID HT013524499
    ISBN 90-5702-645-7 ; 978-90-5702-645-4
    Database Catalogue ZB MED Medicine, Health

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  2. Article ; Online: Immunologic basis for development of keratoconjunctivitis sicca in systemic autoimmune diseases: Role of innate immune sensors.

    Stern, Michael E / Theofilopoulos, Argyrios N / Steven, Philipp / Niederkorn, Jerry Y / Fox, Robert / Calonge, Margarita / Scheid, Christof / Pflugfelder, Stephen C

    The ocular surface

    2024  Volume 32, Page(s) 130–138

    Abstract: The literature is filled with citations reporting an increased incidence of chronic dry eye disease, also known as keratoconjunctivitis sicca, in patients with systemic autoimmune diseases such as rheumatoid arthritis, Sjögren's Syndrome, systemic ... ...

    Abstract The literature is filled with citations reporting an increased incidence of chronic dry eye disease, also known as keratoconjunctivitis sicca, in patients with systemic autoimmune diseases such as rheumatoid arthritis, Sjögren's Syndrome, systemic sclerosis and lupus. As the most environmentally exposed mucosal surface of the body, the conjunctiva constantly responds to environmental challenges which are typically self limited, but when persistent and unresolved may provoke pathogenic innate and adaptive immune reactions. Our understanding of the pathophysiological mechanisms by which systemic autoimmune diseases cause dry eye inducing ocular surface inflammation continues to evolve. Conjunctival immune tone responds to self or foreign danger signals (including desiccating stress) on the ocular surface with an initial non-specific innate inflammatory response. If unchecked, this can lead to activation of dendritic cells that present antigen and prime T and B cells resulting in an adaptive immune reaction. These reactions generally resolve, but dysfunctional, hyper-responsive immune cells found in systemic autoimmune diseases that are recruited to the ocular surface can amplify inflammatory stress responses in the ocular surface and glandular tissues and result in autoimmune reactions that disrupt tear stability and lead to chronic dry eye disease. We here propose that unique features of the ocular surface immune system and the impact of systemic immune dysregulation in autoimmune diseases, can predispose to development of dry eye disease, and exacerbate severity of existing dry eye.
    MeSH term(s) Humans ; Keratoconjunctivitis Sicca/immunology ; Immunity, Innate ; Autoimmune Diseases/immunology ; Conjunctiva/immunology ; Conjunctiva/pathology ; Tears/immunology ; Tears/metabolism
    Language English
    Publishing date 2024-02-22
    Publishing country United States
    Document type Journal Article ; Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2208578-6
    ISSN 1937-5913 ; 1542-0124
    ISSN (online) 1937-5913
    ISSN 1542-0124
    DOI 10.1016/j.jtos.2024.02.003
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Book ; Online: Genes and genetics of autoimmunity

    Theofilopoulos, Argyrios N.

    1999  

    Author's details vol. ed.: A. N. Theofilopoulos
    Language English
    Size VIII + 296 S.
    Publisher Karger
    Publishing place Basel
    Publishing country Switzerland
    Document type Book ; Online
    HBZ-ID TT050388149
    ISBN 978-3-318-00386-4 ; 3-318-00386-7
    Database ZB MED Catalogue: Medicine, Health, Nutrition, Environment, Agriculture

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  4. Book: Genes and genetics of autoimmunity

    Theofilopoulos, Argyrios N.

    27 tables

    (Current directions in autoimmunity ; 1)

    1999  

    Author's details vol. ed. A. N. Theofilopoulos
    Series title Current directions in autoimmunity ; 1
    Collection
    Keywords Autoimmunität ; Genetik ; Autoaggressionskrankheit
    Subject Allgemeine Genetik ; Erbbiologie ; Erbforschung ; Erblehre ; Vererbungslehre ; Vererbungswissenschaft ; Erblichkeitslehre ; Autoantikörperkrankheit ; Autoimmunkrankheit ; Autoimmunopathie ; Autoimmunerkrankung
    Language English
    Size VII, 296 S. : graph. Darst.
    Publisher Karger
    Publishing place Basel u.a.
    Publishing country Switzerland
    Document type Book
    HBZ-ID HT010614811
    ISBN 3-8055-6814-2 ; 978-3-8055-6814-2
    Database Catalogue ZB MED Medicine, Health

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    In stock of ZB MED Cologne/Königswinter

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  5. Article ; Online: TLRs and IFNs: critical pieces of the autoimmunity puzzle.

    Theofilopoulos, Argyrios N

    The Journal of clinical investigation

    2012  Volume 122, Issue 10, Page(s) 3464–3466

    Abstract: Discoveries revealing the molecular basis of innate immune responses, particularly the identification of Toll-like receptors (TLRs) as the major recognition sensors for microbial and even self-molecules, have provided new insights into the pathogenesis ... ...

    Abstract Discoveries revealing the molecular basis of innate immune responses, particularly the identification of Toll-like receptors (TLRs) as the major recognition sensors for microbial and even self-molecules, have provided new insights into the pathogenesis of both systemic and organ-specific autoimmune diseases. These insights will permit the development of novel treatment modalities for these disorders.
    MeSH term(s) Animals ; Animals, Congenic ; Antibodies, Antinuclear/immunology ; Antigen Presentation ; Antigen-Presenting Cells/immunology ; Autoantibodies/immunology ; Autoantigens/immunology ; Autoimmunity/immunology ; Disease Models, Animal ; Endosomes/immunology ; Female ; Humans ; Interferons/immunology ; Isoantigens/immunology ; Lupus Erythematosus, Systemic/drug therapy ; Lupus Erythematosus, Systemic/etiology ; Lupus Erythematosus, Systemic/immunology ; Male ; Mice ; Mice, Knockout ; Nucleic Acids/immunology ; Toll-Like Receptors/immunology
    Chemical Substances Antibodies, Antinuclear ; Autoantibodies ; Autoantigens ; Isoantigens ; Nucleic Acids ; Toll-Like Receptors ; Interferons (9008-11-1)
    Language English
    Publishing date 2012-10-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI63835
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Chemoproteomic development of SLC15A4 inhibitors with anti-inflammatory activity.

    Chiu, Tzu-Yuan / Lazar, Daniel C / Wang, Wesley W / Wozniak, Jacob M / Jadhav, Appaso M / Li, Weichao / Gazaniga, Nathalia / Theofilopoulos, Argyrios N / Teijaro, John R / Parker, Christopher G

    Nature chemical biology

    2024  

    Abstract: SLC15A4 is an endolysosome-resident transporter linked with autoinflammation and autoimmunity. Specifically, SLC15A4 is critical for Toll-like receptors (TLRs) 7-9 as well as nucleotide-binding oligomerization domain-containing protein (NOD) signaling in ...

    Abstract SLC15A4 is an endolysosome-resident transporter linked with autoinflammation and autoimmunity. Specifically, SLC15A4 is critical for Toll-like receptors (TLRs) 7-9 as well as nucleotide-binding oligomerization domain-containing protein (NOD) signaling in several immune cell subsets. Notably, SLC15A4 is essential for the development of systemic lupus erythematosus in murine models and is associated with autoimmune conditions in humans. Despite its therapeutic potential, the availability of quality chemical probes targeting SLC15A4 functions is limited. In this study, we used an integrated chemical proteomics approach to develop a suite of chemical tools, including first-in-class functional inhibitors, for SLC15A4. We demonstrate that these inhibitors suppress SLC15A4-mediated endolysosomal TLR and NOD functions in a variety of human and mouse immune cells; we provide evidence of their ability to suppress inflammation in vivo and in clinical settings; and we provide insights into their mechanism of action. Our findings establish SLC15A4 as a druggable target for the treatment of autoimmune and autoinflammatory conditions.
    Language English
    Publishing date 2024-01-08
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2202962-X
    ISSN 1552-4469 ; 1552-4450
    ISSN (online) 1552-4469
    ISSN 1552-4450
    DOI 10.1038/s41589-023-01527-8
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.MG 90: Show issues

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  7. Article ; Online: The multiple pathways to autoimmunity.

    Theofilopoulos, Argyrios N / Kono, Dwight H / Baccala, Roberto

    Nature immunology

    2017  Volume 18, Issue 7, Page(s) 716–724

    Abstract: Efforts to understand autoimmunity have been pursued relentlessly for several decades. It has become apparent that the immune system evolved multiple mechanisms for controlling self-reactivity, and defects in one or more of these mechanisms can lead to a ...

    Abstract Efforts to understand autoimmunity have been pursued relentlessly for several decades. It has become apparent that the immune system evolved multiple mechanisms for controlling self-reactivity, and defects in one or more of these mechanisms can lead to a breakdown of tolerance. Among the multitude of lesions associated with disease, the most common seem to affect peripheral tolerance rather than central tolerance. The initial trigger for both systemic autoimmune disorders and organ-specific autoimmune disorders probably involves the recognition of self or foreign molecules, especially nucleic acids, by innate sensors. Such recognition, in turn, triggers inflammatory responses and the engagement of previously quiescent autoreactive T cells and B cells. Here we summarize the most prominent autoimmune pathways and identify key issues that require resolution for full understanding of pathogenic autoimmunity.
    MeSH term(s) Animals ; Autoimmune Diseases/immunology ; Autoimmunity/immunology ; B-Lymphocytes/immunology ; Central Tolerance/immunology ; Humans ; Peripheral Tolerance/immunology ; Self Tolerance/immunology ; T-Lymphocytes/immunology
    Language English
    Publishing date 2017-06-20
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2016987-5
    ISSN 1529-2916 ; 1529-2908
    ISSN (online) 1529-2916
    ISSN 1529-2908
    DOI 10.1038/ni.3731
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: The solute carrier SLC15A4 is required for optimal trafficking of nucleic acid-sensing TLRs and ligands to endolysosomes.

    Rimann, Ivo / Gonzalez-Quintial, Rosana / Baccala, Roberto / Kiosses, William B / Teijaro, John R / Parker, Christopher G / Li, Xiaohong / Beutler, Bruce / Kono, Dwight H / Theofilopoulos, Argyrios N

    Proceedings of the National Academy of Sciences of the United States of America

    2022  Volume 119, Issue 14, Page(s) e2200544119

    Abstract: A function-impairing mutation (feeble) or genomic deletion of SLC15A4 abolishes responses of nucleic acid–sensing endosomal toll-like receptors (TLRs) and significantly reduces disease in mouse models of lupus. Here, we demonstrate disease reduction in ... ...

    Abstract A function-impairing mutation (feeble) or genomic deletion of SLC15A4 abolishes responses of nucleic acid–sensing endosomal toll-like receptors (TLRs) and significantly reduces disease in mouse models of lupus. Here, we demonstrate disease reduction in homozygous and even heterozygous Slc15a4 feeble mutant BXSB male mice with a Tlr7 gene duplication. In contrast to SLC15A4, a function-impairing mutation of SLC15A3 did not diminish type I interferon (IFN-I) production by TLR-activated plasmacytoid dendritic cells (pDCs), indicating divergence of function between these homologous SLC15 family members. Trafficking to endolysosomes and function of SLC15A4 were dependent on the Adaptor protein 3 (AP-3) complex. Importantly, SLC15A4 was required for trafficking and colocalization of nucleic acid–sensing TLRs and their ligands to endolysosomes and the formation of the LAMP2+VAMP3+ hybrid compartment in which IFN-I production is initiated. Collectively, these findings define mechanistic processes by which SLC15A4 controls endosomal TLR function and suggest that pharmacologic intervention to curtail the function of this transporter may be a means to treat lupus and other endosomal TLR-dependent diseases.
    MeSH term(s) Animals ; Endosomes/metabolism ; Ligands ; Lysosomes/metabolism ; Membrane Transport Proteins/genetics ; Mice ; Nucleic Acids ; Toll-Like Receptors/metabolism
    Chemical Substances Ligands ; Membrane Transport Proteins ; Nucleic Acids ; Slc15a4 protein, mouse ; Toll-Like Receptors
    Language English
    Publishing date 2022-03-29
    Publishing country United States
    Document type Journal Article
    ZDB-ID 209104-5
    ISSN 1091-6490 ; 0027-8424
    ISSN (online) 1091-6490
    ISSN 0027-8424
    DOI 10.1073/pnas.2200544119
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  9. Article ; Online: Lupus acceleration by a MAVS-activating RNA virus requires endosomal TLR signaling and host genetic predisposition.

    Gonzalez-Quintial, Rosana / Nguyen, Anthony / Kono, Dwight H / Oldstone, Michael B A / Theofilopoulos, Argyrios N / Baccala, Roberto

    PloS one

    2018  Volume 13, Issue 9, Page(s) e0203118

    Abstract: Viruses have long been implicated in the pathogenesis of autoimmunity, yet their contribution remains circumstantial partly due to the lack of well-documented information on infections prior to autoimmune disease onset. Here, we used the lymphocytic ... ...

    Abstract Viruses have long been implicated in the pathogenesis of autoimmunity, yet their contribution remains circumstantial partly due to the lack of well-documented information on infections prior to autoimmune disease onset. Here, we used the lymphocytic choriomeningitis virus (LCMV) as a model to mechanistically dissect the impact of viral infection on lupus-like autoimmunity. Virus persistence strongly enhanced disease in mice with otherwise weak genetic predisposition but not in highly predisposed or non-autoimmune mice, indicating a synergistic interplay between genetic susceptibility and virus infection. Moreover, endosomal Toll-like receptors (TLRs) and plasmacytoid dendritic cells (pDCs) were both strictly required for disease acceleration, even though LCMV also induces strong TLR-independent type I interferon (IFN-I) production via RNA helicases and MAVS in conventional DCs. These results suggest that LCMV enhances systemic autoimmunity primarily by providing stimulatory nucleic acids for endosomal TLR engagement, whereas overstimulation of the MAVS-dependent cytosolic pathway in the absence of endosomal TLR signaling is insufficient for disease induction.
    MeSH term(s) Adaptor Proteins, Signal Transducing/deficiency ; Adaptor Proteins, Signal Transducing/genetics ; Animals ; Autoimmunity/genetics ; Cells, Cultured ; Dendritic Cells/immunology ; Dendritic Cells/virology ; Disease Models, Animal ; Endosomes/immunology ; Endosomes/virology ; Female ; Genetic Predisposition to Disease ; Interferon Type I/metabolism ; Lupus Erythematosus, Systemic/genetics ; Lupus Erythematosus, Systemic/immunology ; Lupus Erythematosus, Systemic/virology ; Lymphocytic Choriomeningitis/genetics ; Lymphocytic Choriomeningitis/immunology ; Lymphocytic choriomeningitis virus ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Signal Transduction ; Toll-Like Receptors/metabolism
    Chemical Substances Adaptor Proteins, Signal Transducing ; IPS-1 protein, mouse ; Interferon Type I ; Toll-Like Receptors
    Language English
    Publishing date 2018-09-10
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0203118
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article: Effector and predisposing genes in murine lupus.

    Theofilopoulos, A N

    Lupus

    1998  Volume 7, Issue 9, Page(s) 575–584

    MeSH term(s) Animals ; Genes/genetics ; Genetic Predisposition to Disease ; Lupus Erythematosus, Systemic/genetics ; Mice
    Language English
    Publishing date 1998
    Publishing country England
    Document type Journal Article ; Research Support, U.S. Gov't, P.H.S. ; Review
    ZDB-ID 1154407-7
    ISSN 0961-2033
    ISSN 0961-2033
    DOI 10.1191/096120398678920686
    Database MEDical Literature Analysis and Retrieval System OnLINE

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