Ligand-Independent Down-Regulation of IFN-γ Receptor 1 Following TCR Engagement
| Autor: | Sidney Pestka, Heidi Skrenta, C. Garrison Fathman, Yang Yang |
|---|---|
| Rok vydání: | 2000 |
| Předmět: |
CD4-Positive T-Lymphocytes
Intracellular Fluid Male Time Factors T cell CD3 Immunology Receptors Antigen T-Cell Down-Regulation Mice Transgenic Biology Ligands Lymphocyte Activation Interferon-gamma Mice medicine Animals Immunology and Allergy Cytotoxic T cell IL-2 receptor Interleukin-7 receptor Cells Cultured Receptors Interferon Common gamma chain Mice Knockout Mice Inbred BALB C Cell Membrane CD28 Molecular biology Cell biology medicine.anatomical_structure biology.protein Female Extracellular Space Cytokine receptor Signal Transduction |
| Zdroj: | The Journal of Immunology. 164:3506-3511 |
| ISSN: | 1550-6606 0022-1767 |
| Popis: | Activated T lymphocytes modulate the level of many molecules on their cell surface, including cytokine receptors. This regulation of cytokine receptor expression affects the ability of T cells to respond to cytokines and thus influences the outcome of an immune response. The receptor for IFN-γ, a proinflammatory cytokine, consists of two copies of a ligand binding chain (IFN-γR1) as well as two copies of a second chain (IFN-γR2) required for signal transduction. The expression of IFN-γR2 is down-regulated at the mRNA level on CD4+ T cells when they differentiate into the Th1, but not the Th2, phenotype. This down-regulation has been demonstrated to depend on the ligand, IFN-γ, which is produced by Th1 but not Th2 T cells. The regulation of the cell-surface expression of IFN-γ receptors during primary T cell activation has not been reported. Naive and differentiated T lymphocytes express IFN-γR1 at the mRNA level and as a cell-surface protein. In this study, we present evidence that cell-surface expression of IFN-γR1 is transiently down-regulated on the surface of naive CD4+ T cells shortly after TCR engagement. Furthermore, this down-regulation is not mediated by the ligand, IFN-γ, but results from TCR engagement and can be inhibited by cyclosporin A. |
| Databáze: | OpenAIRE |
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