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CD8(+)NKT-like cells regulate the immune response by killing antigen-bearing DCs.
| Content Provider | Europe PMC |
|---|---|
| Author | Wang, Chao Liu, Xi Li, Zhengyuan Chai, Yijie Jiang, Yunfeng Wang, Qian Ji, Yewei Zhu, Zhongli Wan, Ying Yuan, Zhenglong Chang, Zhijie Zhang, Minghui |
| Copyright Year | 2015 |
| Abstract | CD1d-dependent NKT cells have been extensively studied; however, the function of CD8(+)NKT-like cells, which are CD1d-independent T cells with NK markers, remains unknown. Here, we report that CD1d-independent CD8(+)NKT-like cells, which express both T cell markers (TCRβ and CD3) and NK cell receptors (NK1.1, CD49b and NKG2D), are activated and significantly expanded in mice immunized with GFP-expressing dendritic cells. Distinct from CD1d-dependent NKT cells, CD8(+)NKT-like cells possess a diverse repertoire of TCRs and secrete high levels of IFN-gamma but not IL-4. CD8(+)NKT-like cell development is normal in CD1d(-/-) mice, which suggests that CD8(+)NKT-like cells undergo a unique development pathway that differs from iNKT cells. Further functional analyses show that CD8(+)NKT-like cells suppress T-cell responses through elimination of dendritic cells in an antigen-specific manner. Adoptive transfer of antigen-specific CD8(+)NKT-like cells into RIP-OVA mice prevented subsequent development of diabetes in the animals induced by activated OT-I CD8 T cells. Our study suggests that CD8(+)NKT-like cells can function as antigen-specific suppressive cells to regulate the immune response through killing antigen-bearing DCs. Antigen-specific down regulation may provide an active and precise method for constraining an excessive immune response and avoiding bypass suppression of necessary immune responses to other antigens. |
| Journal | Scientific Reports [Sci Rep] |
| Volume Number | 5 |
| DOI | 10.1038/srep14124 |
| PubMed Central reference number | PMC4569892 |
| PubMed reference number | 26369936 |
| e-ISSN | 20452322 |
| Language | English |
| Publisher | Nature Publishing Group |
| Publisher Date | 2015-09-15 |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
| Subject | Multidisciplinary |
