| Content Provider |
World Health Organization (WHO)-Global Index Medicus |
| Author |
Tang, Hui Yu, Sen Liu, Yuan-Feng Ge, Qing Zhang, Yu Liu, Chen Wang, Hong-Cheng Jin, Rong Sun, Xiao-Hong |
| Description |
Author Affiliation: Liu C ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China); Wang HC ( Oklahoma Medical Research Foundation, Oklahoma City, OK 73104.); Yu S ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China); Jin R ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China); Tang H ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China); Liu YF ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China); Ge Q ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China); Sun XH ( Oklahoma Medical Research Foundation, Oklahoma City, OK 73104 sunx@omrf.org zhangyu007@bjmu.edu.cn.); Zhang Y ( Department of Immunology, Peking University Health Science Center, Beijing, 100083, China) |
| Abstract |
T regulatory (Treg) cells play crucial roles in the regulation of cellular immunity. The development of Treg cells depends on signals from TCRs and IL-2Rs and is influenced by a variety of transcription factors. The basic helix-loop-helix proteins are known to influence TCR signaling thresholds. Whether this property impacts Treg differentiation is not understood. In this study, we interrogated the role of basic helix-loop-helix proteins in the production of Treg cells using the CD4 promoter-driven Id1 transgene. We found that Treg cells continued to accumulate as Id1 transgenic mice aged, resulting in a significant increase in Treg cell counts in the thymus as well as in the periphery compared with wild-type controls. Data from mixed bone marrow assays suggest that Id1 acts intrinsically on developing Treg cells. We made a connection between Id1 expression and CD28 costimulatory signaling because Id1 transgene expression facilitated the formation of Treg precursors in CD28(-/-) mice and the in vitro differentiation of Treg cells on thymic dendritic cells despite the blockade of costimulation by anti-CD80/CD86. Id1 expression also allowed in vitro Treg differentiation without anti-CD28 costimulation, which was at least in part due to enhanced production of IL-2. Notably, with full strength of costimulatory signals, however, Id1 expression caused modest but significant suppression of Treg induction. Finally, we demonstrate that Id1 transgenic mice were less susceptible to the induction of experimental autoimmune encephalomyelitis, thus illustrating the impact of Id1-mediated augmentation of Treg cell levels on cellular immunity. |
| ISSN |
00221767 |
| e-ISSN |
15506606 |
| DOI |
10.4049/jimmunol.1302554 |
| Journal |
The Journal of Immunology |
| Issue Number |
2 |
| Volume Number |
193 |
| Language |
English |
| Publisher |
The American Association of Immunologists |
| Publisher Date |
2014-07-15 |
| Publisher Place |
United States |
| Access Restriction |
Open |
| Subject Keyword |
Cell Differentiation Immunology Inhibitor Of Differentiation Protein 1 Receptors, Antigen, T-cell T-lymphocytes, Regulatory Animals Antigens, Cd28 Genetics Metabolism Antigens, Cd80 Antigens, Cd86 Cells, Cultured Dendritic Cells Encephalomyelitis, Autoimmune, Experimental Flow Cytometry Forkhead Transcription Factors Interleukin-2 Lymphocyte Count Mice Mice, Inbred C57bl Mice, Knockout Mice, Transgenic Signal Transduction Thymus Gland Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Discipline Immunology |
| Content Type |
Text |
| Resource Type |
Article |
| Subject |
Immunology and Allergy Immunology |
