Involvement of tumor necrosis factor receptor superfamily (TNFRSF) members in the pathogenesis of inflammatory diseases.
- Author:
Byungsuk KWON
1
;
Byung Sam KIM
;
Hong Rae CHO
;
Jeong Euy PARK
;
Byoung Se KWON
Author Information
1. The Immunomodulation Research Center University of Uls an, Ulsan 680-749, Korea. bkwon@mail.ulsan.ac.kr
- Publication Type:Review ; Research Support, Non-U.S. Gov't
- Keywords:
autoimmune diseases;
inflammation;
re-ceptors;
tumor necrosis factor
- MeSH:
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
- From:Experimental & Molecular Medicine
2003;35(1):8-16
- CountryRepublic of Korea
- Language:English
-
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.
