In vivo ligation of glucocorticoid-induced TNF receptor enhances the T-cell immunity to herpes simplex virus type 1.
- Author:
Soojin LA
1
;
Eunhwa KIM
;
Byungsuk KWON
Author Information
1. The Immunomodulation Research Center and Department of Biological Science, University of Ulsan, Ulsan 680-749, Korea. bkwon@mail.ulsan.ac.kr
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
GITR;
HSV-1;
gB;
gD;
Th1 cell;
CTL
- MeSH:
Animals;
Antibodies, Monoclonal/pharmacology;
CD4-Positive T-Lymphocytes/immunology;
CD8-Positive T-Lymphocytes/immunology;
Cell Proliferation;
Female;
Glucocorticoids/*pharmacology;
Herpes Simplex/*immunology;
Herpesvirus 1, Human/pathogenicity;
*Immunity, Cellular;
Interferon Type II/secretion;
*Lymphocyte Activation;
Mice;
Mice, Inbred BALB C;
Peptide Fragments/metabolism;
Receptors, Interleukin-2/metabolism;
Receptors, Nerve Growth Factor/genetics/immunology/*metabolism;
Receptors, Tumor Necrosis Factor/genetics/immunology/*metabolism;
Research Support, Non-U.S. Gov't;
T-Lymphocytes/*immunology/metabolism/virology
- From:Experimental & Molecular Medicine
2005;37(3):193-198
- CountryRepublic of Korea
- Language:English
-
Abstract:
GITR (glucocorticoid-induced TNF receptor) is a recently identified member of the TNF receptor superfamily. The receptor is preferentially expressed on CD4+CD25+ regulatory T cells and GITR signals break the suppressive activity of the subset. In this study, we wanted to reveal the in vivo function of GITR in herpes simplex virus type 1 (HSV-1) infection. A single injection of anti-GITR mAb (DTA-1) immediately after viral infection significantly increased the number of CD4+ and CD8+ T cells expressing CD25, an activation surface marker, and secreting IFN-gamma. We confirmed these in vivo observations by showing ex vivo that re-stimulation of CD4+ or CD8+ T cells with a CD4+ or CD8+ T-cell-specific HSV-1 peptide, respectively, induced a significant elevation in cell proliferation and in IFN-gamma secretion. Our results indicate that GITR signals play a critical role in the T-cell immunity to HSV-1.
