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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Schmaler, Mathias Lagarde, Nadège Rossi, Simona W. Finke, Daniela King, Carolyn G. Stöcklin, Benjamin F. Broggi, Maria A. S. |
| Description | Author Affiliation: Schmaler M ( Department of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland); Broggi MA ( Department of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland); Lagarde N ( Department of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland); Stöcklin BF ( Department of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland); King CG ( Department of Biomedicine, Transplantation Immunology and Nephrology, University of Basel and University Hospital of Basel, Basel 4031, Switzerland); Finke D ( Department of Biomedicine, University of Basel and University Hospital of Basel, Basel 4058, Switzerland.); Rossi SW ( Department of Biomedicine, Immunoregulation, University of Basel and University Hospital of Basel, Basel 4031, Switzerland); |
| Abstract | Foxp3(+)CD4(+) regulatory T cells (Treg) have a crucial role in controlling CD4(+) T-cell activation, proliferation, and effector function. However, the molecular mechanisms regulating Treg function remain poorly understood. Here we assessed the role of IL-7, a key cytokine regulating T-cell homeostasis, in suppressor capacity of Treg. Using a skin allograft model in which transplant acceptance is controlled by the number of transferred Treg, we find that Treg impair the proliferation of allogeneic CD4(+) T cells, decrease production of IFNγ by effector T cells, and prevent early and increase late IL-7 induction by lymph node stromal cells. Increased IL-7 availability enhanced Treg survival, stabilized Treg molecular signature, enhanced surface IL-2R expression, and improved IL-2 binding of Treg, which diminished proliferation of alloreactive CD4(+) T cells. Sequestration of IL-7 or impairment of IL-7R signaling after allograft transplantation abolished Treg-mediated tolerance by limiting their suppressive capacity. Aged Il7r -ΔTreg mice displayed mild symptoms of autoimmunity correlating with impaired expansion of effector Treg in response to IL-2. Thus, IL-7R signaling on Treg supports the functional activity of effector Treg by increasing their IL-2 sensitivity in the lymph node during peripheral and allograft tolerance. |
| ISSN | 00278424 |
| e-ISSN | 10916490 |
| Journal | Proceedings of the National Academy of Sciences of the United States of America |
| Issue Number | 43 |
| Volume Number | 112 |
| Language | English |
| Publisher | National Academy of Sciences |
| Publisher Date | 2015-10-01 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Peripheral Tolerance Immunology Receptors, Interleukin-7 Metabolism Signal Transduction T-Lymphocytes, Regulatory Transplantation Tolerance Animals DNA Primers Genetics Flow Cytometry Histological Techniques Interleukin-2 Lymph Nodes Mice Reverse Transcriptase Polymerase Chain Reaction Skin Transplantation Statistics, Nonparametric Research Support, Non-U.S. Gov't Multidisciplinary |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
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