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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Messer, Ronald J. Carmody, Aaron B. Mak, Tak W. Dittmer, Ulf Lang, Karl S. Lang, Philipp A. Wajant, Harald Myers, Lara Joedicke, Jara J. Hasenkrug, Kim J. |
| Description | Author Affiliation: Joedicke JJ ( Institute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany); Myers L ( Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840); Carmody AB ( Research Technologies Branch, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840); Messer RJ ( Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840); Wajant H ( Division of Molecular Internal Medicine, Department of Internal Medicine II, University Hospital Würzburg, Würzburg 97080, Germany); Lang KS ( Institute for Immunology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany); Lang PA ( Department of Gastroenterology, Hepatology, and Infectious Diseases, Heinrich-Heine-University Düsseldorf, Düsseldorf 40225, Germany); Mak TW ( Department of Medical Biophysics and Immunology, The Campbell Family Institute for Breast Cancer Research, Ontario Cancer Institute, University Health Network, University of Toronto, Toronto, Ontario M5G 2M9, Canada.); Hasenkrug KJ ( Laboratory of Persistent Viral Diseases, Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, MT 59840); Dittmer U ( Institute for Virology, University Hospital Essen, University of Duisburg-Essen, Essen 45147, Germany) |
| Abstract | Vß5(+) regulatory T cells (Tregs), which are specific for a mouse endogenous retroviral superantigen, become activated and proliferate in response to Friend virus (FV) infection. We previously reported that FV-induced expansion of this Treg subset was dependent on CD8(+) T cells and TNF- , but independent of IL-2. We now show that the inflammatory milieu associated with FV infection is not necessary for induction of Vß5(+) Treg expansion. Rather, it is the presence of activated CD8(+) T cells that is critical for their expansion. The data indicate that the mechanism involves signaling between the membrane-bound form of TNF- on activated CD8(+) T cells and TNFR2 on Tregs. CD8(+) T cells expressing membrane-bound TNF- but no soluble TNF- remained competent to induce strong Vß5(+) Treg expansion in vivo. In addition, Vß5(+) Tregs expressing only TNFR2 but no TNFR1 were still responsive to expansion. Finally, treatment of naive mice with soluble TNF- did not induce Vß5(+) Treg expansion, but treatment with a TNFR2-specific agonist did. These results reveal a new mechanism of intercellular communication between activated CD8(+) T cell effectors and Tregs that results in the activation and expansion of a Treg subset that subsequently suppresses CD8(+) T cell functions. |
| ISSN | 00221767 |
| e-ISSN | 15506606 |
| DOI | 10.4049/jimmunol.1400649 |
| Journal | The Journal of Immunology |
| Issue Number | 6 |
| Volume Number | 193 |
| Language | English |
| Publisher | The American Association of Immunologists |
| Publisher Date | 2014-09-15 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Cd8-positive T-lymphocytes Immunology Lymphocyte Activation Receptors, Antigen, T-cell, Alpha-beta Biosynthesis Receptors, Tumor Necrosis Factor, Type Ii Tumor Necrosis Factor-alpha Animals Carrier Proteins Genetics Friend Murine Leukemia Virus Leukemia, Experimental Mice Mice, Inbred C57bl Mice, Knockout Receptors, Tumor Necrosis Factor, Type I Agonists Retroviridae Infections Signal Transduction T-lymphocytes, Regulatory Tumor Virus Infections Research Support, N.i.h., Intramural Research Support, Non-u.s. Gov't Discipline Immunology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Immunology and Allergy Immunology |
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