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Verfasst von:Sobek, Vera [VerfasserIn]   i
 Birkner, Nico [VerfasserIn]   i
 Falk, Ingrid [VerfasserIn]   i
 Würch, Andreas [VerfasserIn]   i
 Kirschning, Carsten J. [VerfasserIn]   i
 Wagner, Hermann [VerfasserIn]   i
 Wallich, Reinhard [VerfasserIn]   i
 Lamers, Marinus C. [VerfasserIn]   i
 Simon, Markus M. [VerfasserIn]   i
Titel:Direct Toll-like receptor 2 mediated co-stimulation of T cells in the mouse system as a basis for chronic inflammatory joint disease
Verf.angabe:Vera Sobek, Nico Birkner, Ingrid Falk, Andreas Würch, Carsten J. Kirschning, Hermann Wagner, Reinhard Wallich, Marinus C. Lamers, and Markus M. Simon
Jahr:2004
Umfang:14 S.
Fussnoten:Gesehen am 24.02.2021
Titel Quelle:Enthalten in: Arthritis Research & Therapy
Ort Quelle:London : BioMed Central, 1999
Jahr Quelle:2004
Band/Heft Quelle:6(2004), 5, Seite R433-446
ISSN Quelle:1465-9913
 1478-6362
Abstract:The pathogenesis of chronic inflammatory joint diseases such as adult and juvenile rheumatoid arthritis and Lyme arthritis is still poorly understood. Central to the various hypotheses in this respect is the notable involvement of T and B cells. Here we develop the premise that the nominal antigen-independent, polyclonal activation of preactivated T cells via Toll-like receptor (TLR)-2 has a pivotal role in the initiation and perpetuation of pathogen-induced chronic inflammatory joint disease. We support this with the following evidence. Both naive and effector T cells express TLR-2. A prototypic lipoprotein, Lip-OspA, from the etiological agent of Lyme disease, namely Borrelia burgdorferi, but not its delipidated form or lipopolysaccharide, was able to provide direct antigen-nonspecific co-stimulatory signals to both antigen-sensitized naive T cells and cytotoxic T lymphocyte (CTL) lines via TLR-2. Lip-OspA induced the proliferation and interferon (IFN)-gamma secretion of purified, anti-CD3-sensitized, naive T cells from C57BL/6 mice but not from TLR-2-deficient mice. Induction of proliferation and IFN-gamma secretion of CTL lines by Lip-OspA was independent of T cell receptor (TCR) engagement but was considerably enhanced after suboptimal TCR activation and was inhibitable by monoclonal antibodies against TLR-2.
DOI:doi:10.1186/ar1212
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext ; Verlag: https://doi.org/10.1186/ar1212
 Volltext: https://arthritis-research.biomedcentral.com/articles/10.1186/ar1212
 DOI: https://doi.org/10.1186/ar1212
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Animals
 Antigens, Surface
 Arthritis, Rheumatoid
 Bacterial Outer Membrane Proteins
 Bacterial Vaccines
 CD8-Positive T-Lymphocytes
 Cell Line
 Cell Proliferation
 Female
 Inflammation
 Interferon-gamma
 Lipoproteins
 Lymphocyte Activation
 Lymphocyte Culture Test, Mixed
 Male
 Membrane Glycoproteins
 Mice
 Mice, Inbred C57BL
 Mice, Inbred Strains
 Receptors, Cell Surface
 Recombinant Proteins
 T-Lymphocyte Subsets
 T-Lymphocytes
 T-Lymphocytes, Cytotoxic
 Toll-Like Receptor 2
 Toll-Like Receptors
K10plus-PPN:174930967X
Verknüpfungen:→ Zeitschrift

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