Role of interferon-γ in Vα14+ natural killer T cell-mediated host defense against Streptococcus pneumoniae infection in murine lungs

2007 ◽  
Vol 9 (3) ◽  
pp. 364-374 ◽  
Author(s):  
Masashi Nakamatsu ◽  
Natsuo Yamamoto ◽  
Masumitsu Hatta ◽  
Chikara Nakasone ◽  
Takeshi Kinjo ◽  
...  
Keyword(s):  
Streptococcus Pneumoniae ◽  
T Cell ◽  
Natural Killer ◽  
Host Defense ◽  
Interferon Γ ◽  
Natural Killer T Cell ◽  
Killer T Cell ◽  
Natural Killer T

scholarly journals Production of Interferon-γ–Inducible Protein-10 and Its Role as an Autocrine Invasion Factor in Nasal Natural Killer/T-Cell Lymphoma Cells

2009 ◽  
Vol 15 (22) ◽  
pp. 6771-6779 ◽  
Author(s):  
Shigetaka Moriai ◽  
Miki Takahara ◽  
Takeshi Ogino ◽  
Toshihiro Nagato ◽  
Kan Kishibe ◽  
...  
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Cell Lymphoma ◽  
Interferon Γ ◽  
T Cell Lymphoma ◽  
Lymphoma Cells ◽  
Natural Killer T Cell ◽  
Inducible Protein ◽  
Killer T Cell ◽  
Natural Killer T

scholarly journals Whole transcriptome analysis reveals dysregulated oncogenic lncRNAs in natural killer/T-cell lymphoma and establishes MIR155HG as a target of PRDM1

Tumor Biology ◽  
2017 ◽  
Vol 39 (5) ◽  
pp. 101042831770164 ◽  
Author(s):  
Esra Baytak ◽  
Qiang Gong ◽  
Burcu Akman ◽  
Hongling Yuan ◽  
Wing C Chan ◽  
...  
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Cell Lymphoma ◽  
Killer Cell ◽  
T Cell Lymphoma ◽  
Natural Killer T Cell ◽  
Non Coding Rnas ◽  
Killer T Cell ◽  
Natural Killer T

Natural killer/T-cell lymphoma is a rare but aggressive neoplasm with poor prognosis. Despite previous reports that showed potential tumor suppressors, such as PRDM1 or oncogenes associated with the etiology of this malignancy, the role of long non-coding RNAs in natural killer/T-cell lymphoma pathobiology has not been addressed to date. Here, we aim to identify cancer-associated dysregulated long non-coding RNAs and signaling pathways or biological processes associated with these long non-coding RNAs in natural killer/T-cell lymphoma cases and to identify the long non-coding RNAs transcriptionally regulated by PRDM1. RNA-Seq analysis revealed 166 and 66 long non-coding RNAs to be significantly overexpressed or underexpressed, respectively, in natural killer/T-cell lymphoma cases compared with resting or activated normal natural killer cells. Novel long non-coding RNAs as well as the cancer-associated ones such as SNHG5, ZFAS1, or MIR155HG were dysregulated. Interestingly, antisense transcripts of many growth-regulating genes appeared to be transcriptionally deregulated. Expression of ZFAS1, which is upregulated in natural killer/T-cell lymphoma cases, showed association with growth-regulating pathways such as stabilization of P53, regulation of apoptosis, cell cycle, or nuclear factor-kappa B signaling in normal and neoplastic natural killer cell samples. Consistent with the tumor suppressive role of PRDM1, we identified MIR155HG and TERC to be transcriptionally downregulated by PRDM1 in two PRDM1-null NK-cell lines when it is ectopically expressed. In conclusion, this is the first study that identified long non-coding RNAs whose expression is dysregulated in natural killer/T-cell lymphoma cases. These findings suggest that ZFAS1 and other dysregulated long non-coding RNAs may be involved in natural killer/T-cell lymphoma pathobiology through regulation of cancer-related genes, and loss-of-PRDM1 expression in natural killer/T-cell lymphomas may contribute to overexpression of MIR155HG; thereby promoting tumorigenesis.

scholarly journals Mapping the Functional Cofactors of Oncogenic EZH2 in Natural Killer/ T Cell Lymphoma (NKTL)

Blood ◽  
2016 ◽  
Vol 128 (22) ◽  
pp. 1773-1773
Author(s):  
Boheng Li ◽  
Junli Yan ◽  
Tae-Hoon Chung ◽  
Pei Tsung Lee ◽  
Wee Joo Chng
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Rna Pol Ii ◽  
Pol Ii ◽  
Natural Killer T Cell ◽  
Killer T Cell ◽  
Natural Killer T

Abstract EZH2, the catalytic subunit of the PRC2 complex, has been shown to overexpress in different types of cancers. Oncogenic role of EZH2 originally was thought to exhibit through its Histone H3 K27 methyltransferase activity. In recent years, several studies, including ours, have highlighted new oncogenic roles of EZH2, either PRC2-independent, or as co-activator for other transcription factors in some context of cancers. Specifically in natural killer/ T cell lymphoma (NKTL), we have already uncovered that oncogenic role of EZH2 is independent of its methyltransferase function, and JAK3 switches EZH2 from a transcriptional repressor to an activator through direct phosphorylation thus conferring the lymphoma cells with growth advantage. What's more, we showed that JAK3, EZH2 and RNA POL II are in the same complex, whereas JAK3 does not stay together with PRC2 complex. In this study, in order to map all the interacting partners of PRC2 complex as well as EZH2-POL II complex, we used NKTL cell lines for SILAC Mass Spectrometry to identify interactome of EZH2, RNA POL II and PRC2 component SUZ12, respectively. Then we overlapped EZH2 and SUZ12 interactome for canonical factors assisting PRC2-mediated gene repression, as well as EZH2 and POL II interactome for non-canonical factors which might play a role in EZH2-regulated gene activation. Some of those non-canonical factors have been shown to display extraordinary high expression in EBV-positive lymphocytes among other cancerous and normal tissues (GTEx RNA-seq expression data), or in NKTL patient sample than normal NK cells (our own GEP data). Intriguingly, GO analysis of these three interactomes indicates that the major function of EZH2 in NKTL is realized mainly through the EZH2-POL II complex, rather than the PRC2 complex. These data reinforced the oncogenic role of EZH2-POL II complex in NKTL, and suggested new players in EZH2-mediated oncogenesis. Disclosures No relevant conflicts of interest to declare.

scholarly journals Superior Protection against Malaria and Melanoma Metastases by a C-glycoside Analogue of the Natural Killer T Cell Ligand α-Galactosylceramide

2003 ◽  
Vol 198 (11) ◽  
pp. 1631-1641 ◽  
Author(s):  
John Schmieg ◽  
Guangli Yang ◽  
Richard W. Franck ◽  
Moriya Tsuji
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Therapeutic Option ◽  
Interferon Γ ◽  
Th2 Cytokines ◽  
Natural Killer T Cell ◽  
Melanoma Metastases ◽  
Killer T Cell ◽  
Natural Killer T

α-Galactosylceramide (α-GalCer) is a glycolipid that stimulates natural killer T cells to produce both T helper (Th) 1 and Th2 cytokines. This property enables α-GalCer to ameliorate a wide variety of infectious, neoplastic, and autoimmune diseases; however, its effectiveness against any one disease is limited by the opposing activities of the induced Th1 and Th2 cytokines. Here, we report that a synthetic C-glycoside analogue of α-GalCer, α-C-galactosylceramide (α-C-GalCer), acts as natural killer T cell ligand in vivo, and stimulates an enhanced Th1-type response in mice. In two disease models requiring Th1-type responses for control, namely malaria and melanoma metastases, α-C-GalCer exhibited a 1,000-fold more potent antimalaria activity and a 100-fold more potent antimetastatic activity than α-GalCer. Moreover, α-C-GalCer consistently stimulated prolonged production of the Th1 cytokines interferon-γ and interleukin (IL)-12, and decreased production of the Th2 cytokine IL-4 compared with α-GalCer. Finally, α-C-GalCer's enhanced therapeutic activity required the presence of IL-12, which was needed to stimulate natural killer cells for optimal interferon-γ production, but did not affect IL-4. Overall, our results suggest that α-C-GalCer may one day be an excellent therapeutic option for diseases resolved by Th1-type responses.

Differential Role of Natural Killer T Cell Subsets in Xenobiotics-Induced Hepatic Inflammation and Fibrogenesis

2011 ◽  
Vol 140 (5) ◽  
pp. S-929
Author(s):  
Kenichi Ikejima ◽  
Sachiko Ishikawa ◽  
Satoko Hosoya ◽  
Hisafumi Yamagata ◽  
Kumiko Arai ◽  
...  
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
T Cell Subsets ◽  
Hepatic Inflammation ◽  
Natural Killer T Cell ◽  
Killer T Cell ◽  
Natural Killer T

scholarly journals NON-CANONICAL ROLE OF EZH2 IN NATURAL KILLER / T-CELL LYMPHOMA

2017 ◽  
Vol 35 ◽  
pp. 121-122 ◽  
Author(s):  
W.J. Chng ◽  
J. Yan ◽  
B. Li ◽  
B. Lin ◽  
S.B. Ng
Keyword(s):  
T Cell ◽  
Natural Killer ◽  
Cell Lymphoma ◽  
T Cell Lymphoma ◽  
Natural Killer T Cell ◽  
Killer T Cell ◽  
Natural Killer T
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