学術雑誌論文 Strong TCR-mediated signals suppress integrated stress responses induced by KDELR1 deficiency in naive T cells
Strong TCR-mediated signals suppress integrated stress responses induced by KDELR1 deficiency in naïve T cells
A link between TCR-mediated signals and stress responses

Kamimura, Daisuke  ,  Arima, Yasunobu  ,  Tsuruoka, Mineko  ,  Jiang, Jing-jing  ,  Bando, Hidenori  ,  Meng, Jie  ,  Sabharwal, Lavannya  ,  Stofkova, Andrea  ,  Nishikawa, Naoki  ,  Higuchi, Kotaro  ,  Ogura, Hideki  ,  Atsumi, Toru  ,  Murakami, Masaaki

28 ( 3 )  , pp.117 - 126 , 2016-03 , Oxford University Press
ISSN:0953-8178
NII書誌ID(NCID):AA10730708
内容記述
KDEL receptor 1 (KDELR1) regulates integrated stress responses (ISR) to promote naive T-cell survival in vivo. In a mouse line having nonfunctional KDELR1, T-Red (naive T-cell reduced) mice, polyclonal naive T cells show excessive ISR and eventually undergo apoptosis. However, breeding T-Red mice with TCR-transgenic mice bearing relatively high TCR affinity rescued the T-Red phenotype, implying a link between ISR-induced apoptosis and TCR-mediated signaling. Here, we showed that strong TCR stimulation reduces ISR in naive T cells. In mice lacking functional KDELR1, surviving naive T cells expressed significantly higher levels of CD5, a surrogate marker of TCR self-reactivity. In addition, higher TCR affinity/avidity was confirmed using a tetramer dissociation assay on the surviving naive T cells, suggesting that among the naive T-cell repertoire, those that receive relatively stronger TCR-mediated signals via self-antigens survive enhanced ISR. Consistent with this observation, weak TCR stimulation with altered peptide ligands decreased the survival and proliferation of naive T cells, whereas stimulation with ligands having higher affinity had no such effect. These results suggest a novel role of TCR-mediated signals in the attenuation of ISR in vivo.
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http://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/63137/4/Supplementary_Figures_legends.docx

http://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/63137/3/Supplementary_figure1-6.pdf

http://eprints.lib.hokudai.ac.jp/dspace/bitstream/2115/63137/1/IntImmunol28_117.pdf

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