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

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

Research highlights ► EBV increased the expression of IDO on B cells during infection. ► EBV-induced IDO could modulate expression of NK cell-activation receptor, NKG2D via inhibition of c-Jun N-terminal kinase. ► JNK activation can enhance to improve NKG2D expression reduced by IDO metabolite in NK...

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Veröffentlicht in:Immunology letters 2011-05, Vol.136 (2), p.187-193
Hauptverfasser: 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
Format: Artikel
Sprache:eng
Schlagworte:
Allergy and Immunology
Animals
Anisomycin
B-Lymphocytes - immunology
B-Lymphocytes - pathology
c-Jun amino-terminal kinase
Cell Line, Tumor
Cell surface
Culture Media, Conditioned
Cytomegalovirus
Cytotoxicity, Immunologic
Data processing
Down-Regulation - immunology
Epstein-Barr virus
Herpesvirus 4, Human - physiology
Human immunodeficiency virus 1
Humans
IDO
Indoleamine-Pyrrole 2,3,-Dioxygenase - immunology
Infection
Interleukin 18
JNK Mitogen-Activated Protein Kinases - metabolism
K562 Cells
Killer Cells, Natural - enzymology
Killer Cells, Natural - immunology
L-kynurenine
Lymphocytes B
Metabolites
Natural killer cells
NK Cell Lectin-Like Receptor Subfamily K - metabolism
NKG2 antigen
NKG2D
Receptor mechanisms
Signal transduction
Signal Transduction - immunology
Tumor cells
Tumor immunity
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Zusammenfassung:Research highlights ► EBV increased the expression of IDO on B cells during infection. ► EBV-induced IDO could modulate expression of NK cell-activation receptor, NKG2D via inhibition of c-Jun N-terminal kinase. ► JNK activation can enhance to improve NKG2D expression reduced by IDO metabolite in NK cells during infection of EBV.
ISSN:0165-2478
1879-0542
DOI:10.1016/j.imlet.2011.01.009