Cutting Edge: IL-2 Signals Determine the Degree of TCR Signaling Necessary To Support Regulatory T Cell Proliferation In Vivo
| Autor: | Michael A. Farrar, Evann Corbo-Rodgers, Atsushi Satake, Jonathan S. Maltzman, Amanda M. Schmidt, Taku Kambayashi, Tao Zou |
|---|---|
| Rok vydání: | 2012 |
| Předmět: |
CD4-Positive T-Lymphocytes
Interleukin 2 Cell division Regulatory T cell Immunology Antigen presentation Receptors Antigen T-Cell Mice Transgenic chemical and pharmacologic phenomena Biology T-Lymphocytes Regulatory Article Immune tolerance Mice medicine Animals Homeostasis Immunology and Allergy Cell Proliferation Mice Knockout Antigen Presentation Cell growth T-cell receptor Receptors Interleukin-2 hemic and immune systems Adoptive Transfer Cell biology medicine.anatomical_structure Interleukin-2 Signal transduction Cell Division Signal Transduction medicine.drug |
| Zdroj: | The Journal of Immunology. 189:28-32 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.1200507 |
| Popis: | To ensure immune tolerance, regulatory T cell (Treg) numbers must be maintained by cell division. This process has been thought to be strictly dependent on the Treg TCR interacting with MHC class II. In this study, we report that Treg division does not absolutely require cell-autonomous TCR signaling in vivo, depending on the degree of IL-2–mediated stimulation provided. At steady state IL-2 levels, Tregs require cell-autonomous TCR signaling to divide. However, when given exogenous IL-2 or when STAT5 is selectively activated in Tregs, Treg division can occur independently of MHC class II and TCR signaling. Thus, depending on the amount of IL-2R stimulation, a wide range of TCR signals supports Treg division, which may contribute to preservation of a diverse repertoire of Treg TCR specificities. These findings also have therapeutic implications, as TCR signaling by Tregs may not be required when using IL-2 to increase Treg numbers for treatment of inflammatory disorders. |
| Databáze: | OpenAIRE |
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