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Involvement of tumor necrosis factor receptor superfamily (TNFRSF) members in the pathogenesis of inflammatory diseases
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  • Open Access
  • Published: 01 February 2003

Involvement of tumor necrosis factor receptor superfamily (TNFRSF) members in the pathogenesis of inflammatory diseases

  • Byungsuk Kwon1,
  • Byung-Sam Kim,
  • Hong Rae Cho,
  • Jeong-Euy Park &
  • …
  • Byoung Se Kwon 

Experimental & Molecular Medicine volume 35, pages 8–16 (2003)Cite this article

  • 689 Accesses

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Abstract

Current therapies for autoimmune diseases are not cures but merely palliatives, aimed at reducing symptoms. For the most part, these treatments provide nonspecific suppression of the immune system and thus do not distinguish between a pathogenic autoimmune response and a protective immune response. Recently emerging evidence not only has indicated the involvement of members of the TNF receptor/ligand superfamilies but also has revealed exciting innovative strategies for the treatment of autoimmune diseases and other chronic inflammatory diseases without depressing the immune response in general. In this review, we will discuss the regulatory mechanisms of TNF receptor/ligand family members, such as HVEM/ LIGHT, 4-1BB/4-1BBL, and GITR/GITRL that regulate T and B cell functions and participate in the process of inflammatory diseases. We will also discuss how intervening in the costimulatory pathways mediated by these molecules might have some potential as a therapeutic approach to immune disorders.

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  1. The Immunomodulation Research Center, University of Ulsan, Ulsan, 680-749, Korea

    Byungsuk Kwon

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  1. Byungsuk Kwon
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This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

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Kwon, B., Kim, BS., Cho, H. et al. Involvement of tumor necrosis factor receptor superfamily (TNFRSF) members in the pathogenesis of inflammatory diseases. Exp Mol Med 35, 8–16 (2003). https://doi.org/10.1038/emm.2003.2

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  • Published: 01 February 2003

  • Issue Date: 01 February 2003

  • DOI: https://doi.org/10.1038/emm.2003.2

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Keywords

  • autoimmune diseases
  • inflammation
  • receptors
  • tumor necrosis factor

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Experimental & Molecular Medicine (Exp Mol Med) ISSN 2092-6413 (online) ISSN 1226-3613 (print)

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