Exp Mol Med.  2003 Feb;35(1):8-16.

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

Affiliations
  • 1The Immunomodulation Research Center University of Uls an, Ulsan 680-749, Korea. bkwon@mail.ulsan.ac.kr
  • 2Samsung Biomedical Research Institute, Sungkyunkwan University School of Medicine, Seoul 135-710, Korea.
  • 3Cardiology Division Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 135-710, Korea.

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.

Keyword

autoimmune diseases; inflammation; re-ceptors; tumor necrosis factor

MeSH Terms

Animals
Apoptosis
Autoimmune Diseases/immunology/metabolism/pathology
B-Lymphocytes/immunology/physiology
Dendritic Cells/physiology
Human
Inflammation/*immunology
Lymphocyte Activation/immunology
Models, Biological
Receptors, Tumor Necrosis Factor/*physiology
T-Lymphocytes/immunology/physiology
Tumor Necrosis Factor/immunology/*physiology
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