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
- Authors
- Song, Hyunkeun; Park, Hyunjin; Kim, Jiyoung; Park, Gabin; Kim, Yeong-Seok; Kim, Sung Mok; Kim, Daejin; Seo, Su Kil; Lee, Hyun-Kyung; Cho, DaeHo; Hur, Daeyoung
- Issue Date
- May-2011
- Publisher
- ELSEVIER SCIENCE BV
- Keywords
- IDO; L-kynurenine; Natural killer cells; Tumor immunity; NKG2D
- Citation
- IMMUNOLOGY LETTERS, v.136, no.2, pp 187 - 193
- Pages
- 7
- Journal Title
- IMMUNOLOGY LETTERS
- Volume
- 136
- Number
- 2
- Start Page
- 187
- End Page
- 193
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/12583
- DOI
- 10.1016/j.imlet.2011.01.009
- ISSN
- 0165-2478
1879-0542
- 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 100 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. Crown Copyright (C) 2011 Published by Elsevier B.V. All rights reserved.
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