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  Direct Toll-like receptor 2 mediated co-stimulation of T cells in the mouse system as a basis for chronic inflammatory joint disease

Sobek, V., Birkner, N., Falk, I., Würch, A., Kirschning, C. J., Wagner, H., et al. (2004). Direct Toll-like receptor 2 mediated co-stimulation of T cells in the mouse system as a basis for chronic inflammatory joint disease. Arthritis Research & Therapy, 6, R433-R446.

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 Creators:
Sobek, Vera1, Author           
Birkner, Nico1, Author           
Falk, Ingrid1, Author           
Würch, Andreas2, Author           
Kirschning, Carsten J., Author
Wagner, Hermann, Author
Wallich, Reinhard3, Author
Lamers, Marinus C.4, Author           
Simon, Markus M.4, Author           
Affiliations:
1Emeritus Group: Cellular Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243649              
2Department of Developmental Immunology, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243647              
3Max Planck Society, ou_persistent13              
4Metchnikoff Laboratory, Max Planck Institute of Immunobiology and Epigenetics, Max Planck Society, ou_2243654              

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Free keywords: co-stimulation; lipoproteins; rheumatoid arthritis; T lymphocytes; Toll-like receptors
 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)-γ 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-γ 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.

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Language(s): eng - English
 Dates: 2004-07-19
 Publication Status: Published in print
 Pages: -
 Publishing info: -
 Table of Contents: -
 Rev. Type: -
 Identifiers: eDoc: 216116
 Degree: -

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Title: Arthritis Research & Therapy
Source Genre: Journal
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Publ. Info: -
Pages: - Volume / Issue: 6 Sequence Number: - Start / End Page: R433 - R446 Identifier: -