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CD8+NKT-like cells regulate the immune response by killing antigen-bearing DCs.
- Source :
- Scientific Reports; 9/18/2015, p14124, 1p
- Publication Year :
- 2015
-
Abstract
- CD1d-dependent NKT cells have been extensively studied; however, the function of CD8<superscript>+</superscript>NKT-like cells, which are CD1d-independent T cells with NK markers, remains unknown. Here, we report that CD1d-independent CD8<superscript>+</superscript>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<superscript>+</superscript>NKT-like cells possess a diverse repertoire of TCRs and secrete high levels of IFN-gamma but not IL-4. CD8<superscript>+</superscript>NKT-like cell development is normal in CD1d<superscript>−/−</superscript> mice, which suggests that CD8<superscript>+</superscript>NKT-like cells undergo a unique development pathway that differs from iNKT cells. Further functional analyses show that CD8<superscript>+</superscript>NKT-like cells suppress T-cell responses through elimination of dendritic cells in an antigen-specific manner. Adoptive transfer of antigen-specific CD8<superscript>+</superscript>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<superscript>+</superscript>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. [ABSTRACT FROM AUTHOR]
- Subjects :
- IMMUNE response
IMMUNOLOGY
T cells
LYMPHOCYTES
CELL-mediated lympholysis
Subjects
Details
- Language :
- English
- ISSN :
- 20452322
- Database :
- Complementary Index
- Journal :
- Scientific Reports
- Publication Type :
- Academic Journal
- Accession number :
- 109534343
- Full Text :
- https://doi.org/10.1038/srep14124