Induction of interleukin-2 unresponsiveness and down-regulation of the JAK-STAT system upon activation through the T cell receptor
| Autor: | Machie Sakuma, Shoichiro Miyatake, Takashi Saito |
|---|---|
| Rok vydání: | 1997 |
| Předmět: |
Interleukin 2
T-Lymphocytes Immunology Receptors Antigen T-Cell Down-Regulation Mice Transgenic Biology Lymphocyte Activation Mice Interleukin 21 Cyclins Immune Tolerance STAT5 Transcription Factor medicine Animals Immunology and Allergy Cytotoxic T cell IL-2 receptor Cyclin D3 Mice Inbred BALB C Mice Inbred C3H ZAP70 Janus kinase 3 T-cell receptor Janus Kinase 3 CD28 Protein-Tyrosine Kinases Milk Proteins Clone Cells Cell biology DNA-Binding Proteins Gene Expression Regulation Proto-Oncogene Proteins c-bcl-2 Trans-Activators Cancer research Interleukin-2 Cell Division Signal Transduction medicine.drug |
| Zdroj: | ResearcherID |
| ISSN: | 1521-4141 0014-2980 |
| DOI: | 10.1002/eji.1830270733 |
| Popis: | Full activation of T cells with antigen (Ag) and antigen-presenting cells initiates effector functions and proliferation. When T cells are re-stimulated through the T cell receptor (TCR) after a primary stimulation with Ag, growth arrest and cell death are induced. Activation of a T cell clone by cross-linking of TCR induces interleukin (IL)-2 unresponsiveness and ultimately cell death. While the proliferative signal delivered by IL-2 induces c-myc, bcl-2 and cyclin D3 expression, the expression of bcl-2 and cyclin D3 is completely suppressed upon TCR stimulation. Furthermore, TCR stimulation induces a decrease in the protein levels of JAK3 and STAT5, suggesting that IL-2 unresponsiveness and growth arrest of T cells result from down-regulation of JAK3 and STAT5. |
| Databáze: | OpenAIRE |
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