Expression of 4-1BB and 4-1BBL in Graves'Disease.
10.3803/jkes.2006.21.2.116
- Author:
Eun Sook KIM
1
;
Hyo Won JUNG
;
Il Sung NAM-GOONG
;
Soon Joo WOO
;
Jung Il CHOI
;
Young Il KIM
Author Information
1. Department of Internal Medicine, Ulsan University Hospital, College of Medicine, Korea.
- Publication Type:Original Article
- Keywords:
Costimulatory molecule;
Graves' disease;
4-1BB;
4-1BBL
- MeSH:
Antigen-Presenting Cells;
Autoimmune Diseases;
B-Lymphocytes;
Dendritic Cells;
Enzyme-Linked Immunosorbent Assay;
Flow Cytometry;
Graves Disease;
Humans;
Immunoglobulins;
Monocytes;
T-Lymphocytes
- From:Journal of Korean Society of Endocrinology
2006;21(2):116-124
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
BACKGROUND: 4-1BB mediated costimulatory signal is a recently identified immunotherapeutic strategy for treating autoimmune diseases without depressing the immune response. In this study, we investigated the expression of 4-1BB and 4-1BBL on the peripheral blood mononuclear cells (PBMC) and we assessed whether the serum levels of soluble (s) 4-1BB and s4-1BBL in the patients with Graves' disease (GD) and compared them with normal subjects. METHODS: Expression of 4-1BB and 4-1BBL on PBMC of GD patients was determined by flow cytometry. The concentrations of s4-1BB and s4-1BBL were assessed in the sera of GD patients by performing ELISA. RESULTS: 4-1BB was constitutively expressed on naive CD4+ and CD8+ T cells of the GD patients and this was increased by stimulation. 4-1BBL was also expressed on the antigen-presenting cells such as CD19+ B cells, monocytes and dendritic cells in GD patients. The serum levels of s4-1BB and s4-1BBL were significantly higher in GD patients than those in controls, and these levels were significantly correlated with the serum levels of thyroid-binding inhibitory immunoglobulin and free T4. CONCLUSION: These results indicate that effector T cells of GD patients can be activated through the 4-1BB-mediated costimulatory signal. Elevated s4-1BB and s4-1BBL levels in the sera of GD patients may affect modulation of the clinical course in GD patients.
