In vivo ligation of glucocorticoid-induced TNF receptor enhances the T-cell immunity to herpes simplex virus type 1
| Autor: | Byungsuk Kwon, Soojin La, Eunhwa Kim |
|---|---|
| Rok vydání: | 2005 |
| Předmět: |
CD4-Positive T-Lymphocytes
T-Lymphocytes Clinical Biochemistry Herpesvirus 1 Human Receptors Nerve Growth Factor Biology CD8-Positive T-Lymphocytes medicine.disease_cause Lymphocyte Activation Biochemistry Receptors Tumor Necrosis Factor Interferon-gamma Mice In vivo Glucocorticoid-Induced TNFR-Related Protein medicine Animals Secretion IL-2 receptor Receptor Molecular Biology Glucocorticoids Cell Proliferation Immunity Cellular Mice Inbred BALB C Antibodies Monoclonal Herpes Simplex Receptors Interleukin-2 Molecular biology Peptide Fragments Herpes simplex virus Molecular Medicine Female Glucocorticoid CD8 Ex vivo medicine.drug |
| Zdroj: | Experimentalmolecular medicine. 37(3) |
| ISSN: | 1226-3613 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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