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10.4049/jimmunol.1402042 http://scihub22266oqcxt.onion/10.4049/jimmunol.1402042 C4201958!4201958 !25261481     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25261481 &cmd=llinks): Failed to open stream: HTTP request failed! 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Cutting edge: Discrete functions of mTOR signaling in invariant NKT cell development and NKT17 fate decision |pdf=|usr=}}{{25261481 }} gab.com Text Cutting edge: Discrete functions of mTOR signaling in invariant NKT cell development and NKT17 fate decision JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25261481 #FOAvip Invariant NKT (iNKT) cells recently were classified into NKT1, NKT2, and NKT17 lineages with distinct transcription factor and cytokine profiles, but the mechanisms underlying such fate decisions remain elusive. In this article, we report crucial roles for mechanistic target of rapamycin (mTOR) signaling, especially mTORC2, in iNKT cell development and fate determination of NKT17 cells. Loss of Rictor, an obligatory component of mTORC2, decreased thymic and peripheral iNKT cells, which was associated with defective survival. Strikingly, Rictor deficiency selectively abolished the NKT17 lineage, as indicated by a marked reduction in ROR?t and IL-17 expression. Moreover, deletion of phosphatase and tensin homolog (Pten) upregulated mTORC2 activity and enhanced NKT17 generation, but concomitant loss of Rictor reversed the NKT17 dysregulation. In contrast, mTORC1 regulators Raptor and Rheb are dispensable for NKT17 differentiation, despite their importance in iNKT cell thymic development. Our findings establish pivotal and unique roles for mTORC2 signaling, which is reciprocally regulated by Rictor and Pten, in NKT17 lineage determination. Twit Text FOAVip Cutting edge: Discrete functions of mTOR signaling in invariant NKT cell development and NKT17 fate decision ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25261481 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25261481 #FOAvip English Wikipedia <ref>{{Cite pmid|25261481 }}</ref> Cutting edge: Discrete functions of mTOR signaling in invariant NKT cell development and NKT17 fate decision #MMPMID25261481 Wei J ; Yang K ; Chi H J Immunol 2014[Nov]; 193 (9 ): 4297-4301 PMID25261481 show ga Invariant NKT (iNKT) cells recently were classified into NKT1, NKT2, and NKT17 lineages with distinct transcription factor and cytokine profiles, but the mechanisms underlying such fate decisions remain elusive. In this article, we report crucial roles for mechanistic target of rapamycin (mTOR) signaling, especially mTORC2, in iNKT cell development and fate determination of NKT17 cells. Loss of Rictor, an obligatory component of mTORC2, decreased thymic and peripheral iNKT cells, which was associated with defective survival. Strikingly, Rictor deficiency selectively abolished the NKT17 lineage, as indicated by a marked reduction in ROR?t and IL-17 expression. Moreover, deletion of phosphatase and tensin homolog (Pten) upregulated mTORC2 activity and enhanced NKT17 generation, but concomitant loss of Rictor reversed the NKT17 dysregulation. In contrast, mTORC1 regulators Raptor and Rheb are dispensable for NKT17 differentiation, despite their importance in iNKT cell thymic development. Our findings establish pivotal and unique roles for mTORC2 signaling, which is reciprocally regulated by Rictor and Pten, in NKT17 lineage determination. |*Cell Differentiation [MESH] |*Signal Transduction [MESH] |Animals [MESH] |Carrier Proteins/genetics/metabolism [MESH] |Cell Lineage/genetics [MESH] |Immunophenotyping [MESH] |Mice [MESH] |Mice, Knockout [MESH] |Natural Killer T-Cells/*cytology/immunology/*metabolism [MESH] |PTEN Phosphohydrolase/deficiency/genetics/metabolism [MESH] |Rapamycin-Insensitive Companion of mTOR Protein [MESH] |T-Lymphocyte Subsets/*cytology/immunology/*metabolism [MESH]Cutting edge: Discrete functions of mTOR signaling in invariant NKT ce(epmc).pdf DeepDyve Pubget Overpricing