Back to Search
Start Over
IDO metabolite produced by EBV-transformed B cells inhibits surface expression of NKG2D in NK cells via the c-Jun N-terminal kinase (JNK) pathway
- Source :
-
Immunology Letters . May2011, Vol. 136 Issue 2, p187-193. 7p. - Publication Year :
- 2011
-
Abstract
- Abstract: Natural Killer cells are known to play a major role in the innate immune response against viral infections and tumor cells. Several viruses, such as CMV, EBV and HIV-1, have acquired strategies to escape elimination by NK cells. In this study, we observed that EBV infection increased expression of IDO on B cells. To evaluate the function of IDO associated with EBV infection, we investigated whether EBV-induced IDO could modulate expression of NK cell-activation receptor, NKG2D. When NK cells were co-incubated with EBV transformed B cells, surface expression of NKG2D was significantly reduced in NK cells. Incubation with L-kynurenine, an IDO metabolite, down-modulated NKG2D expression in NK cells in a dose- and time-dependent manner. Incubation with the JNK inhibitor SP600125 also inhibited NKG2D expression in NK cells. In addition, we observed that the effect of L-kynurenine was blocked by JNK agonist, anisomycin, suggesting the involvement of the JNK pathway in the signal transduction of L-kynurenine-reduced NKG2D expression. Furthermore, IL-18 significantly reduced L-kynurenine-induced down-regulation of NKG2D expression in NK cells. Taken together, these data indicate that down-regulation of NKG2D by EBV-induced IDO metabolite provides a potential mechanism by which EBV escapes NKG2D-mediated attack by immune cells. [Copyright &y& Elsevier]
- Subjects :
- *PYRROLES
*METABOLITES
*B cells
*GENE expression
*KILLER cells
*KYNURENINE
Subjects
Details
- Language :
- English
- ISSN :
- 01652478
- Volume :
- 136
- Issue :
- 2
- Database :
- Academic Search Index
- Journal :
- Immunology Letters
- Publication Type :
- Academic Journal
- Accession number :
- 59640140
- Full Text :
- https://doi.org/10.1016/j.imlet.2011.01.009