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000143809 0247_ $$2doi$$a10.1016/j.immuni.2019.03.005
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000143809 1001_ $$0P:(DE-He78)bf88e5f49a614f52ba8ce2cd433e6b41$$aWu, Jingxia$$b0$$eFirst author
000143809 245__ $$aLoss of Neurological Disease HSAN-I-Associated Gene SPTLC2 Impairs CD8+ T Cell Responses to Infection by Inhibiting T Cell Metabolic Fitness.
000143809 260__ $$aNew York, NY$$bElsevier$$c2019
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000143809 520__ $$aPatients with the neurological disorder HSAN-I suffer frequent infections, attributed to a lack of pain sensation and failure to seek care for minor injuries. Whether protective CD8+ T cells are affected in HSAN-I patients remains unknown. Here, we report that HSAN-I-associated mutations in serine palmitoyltransferase subunit SPTLC2 dampened human T cell responses. Antigen stimulation and inflammation induced SPTLC2 expression, and murine T-cell-specific ablation of Sptlc2 impaired antiviral-T-cell expansion and effector function. Sptlc2 deficiency reduced sphingolipid biosynthetic flux and led to prolonged activation of the mechanistic target of rapamycin complex 1 (mTORC1), endoplasmic reticulum (ER) stress, and CD8+ T cell death. Protective CD8+ T cell responses in HSAN-I patient PBMCs and Sptlc2-deficient mice were restored by supplementing with sphingolipids and pharmacologically inhibiting ER stress-induced cell death. Therefore, SPTLC2 underpins protective immunity by translating extracellular stimuli into intracellular anabolic signals and antagonizes ER stress to promote T cell metabolic fitness.
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000143809 7001_ $$0P:(DE-He78)b74df323e3939b563635a2cba7a7afba$$aMa, Sicong$$b1$$eFirst author
000143809 7001_ $$0P:(DE-He78)a928ded2085c8911822370cad0b4a728$$aSandhoff, Roger$$b2$$eFirst author
000143809 7001_ $$aMing, Yanan$$b3
000143809 7001_ $$0P:(DE-He78)2f34b89d62d5e5c651aa1e683844b092$$aHotz-Wagenblatt, Agnes$$b4
000143809 7001_ $$aTimmerman, Vincent$$b5
000143809 7001_ $$aBonello-Palot, Nathalie$$b6
000143809 7001_ $$aSchlotter-Weigel, Beate$$b7
000143809 7001_ $$aAuer-Grumbach, Michaela$$b8
000143809 7001_ $$aSeeman, Pavel$$b9
000143809 7001_ $$aLöscher, Wolfgang N$$b10
000143809 7001_ $$aReindl, Markus$$b11
000143809 7001_ $$aWeiss, Florian$$b12
000143809 7001_ $$aMah, Eric$$b13
000143809 7001_ $$0P:(DE-He78)4e185694e1e726dc738bad0a0c41cdd0$$aWeisshaar, Nina$$b14
000143809 7001_ $$0P:(DE-He78)f05eabc961bc296c088b3510d6429d02$$aMadi, Alaa$$b15
000143809 7001_ $$0P:(DE-He78)6c644df06759d9295db52a00eac44c0f$$aMohr, Kerstin$$b16
000143809 7001_ $$0P:(DE-He78)f0981e2f445e4057d7b16b07b3317df3$$aSchlimbach, Tilo$$b17
000143809 7001_ $$0P:(DE-HGF)0$$aVelasco Cárdenas, Rubí M-H$$b18
000143809 7001_ $$0P:(DE-He78)e1ead319ffbadb46745d1edb5363dcb3$$aKoeppel, Jonas$$b19
000143809 7001_ $$0P:(DE-He78)44a64e50f2668a630716e311870d57f2$$aGrünschläger, Florian$$b20
000143809 7001_ $$0P:(DE-HGF)0$$aMüller, Lisann$$b21
000143809 7001_ $$0P:(DE-HGF)0$$aBaumeister, Maren$$b22
000143809 7001_ $$aBrügger, Britta$$b23
000143809 7001_ $$aSchmitt, Michael$$b24
000143809 7001_ $$aWabnitz, Guido$$b25
000143809 7001_ $$aSamstag, Yvonne$$b26
000143809 7001_ $$0P:(DE-He78)0b7ce76033a6756b91f5bfb12602e20b$$aCui, Guoliang$$b27$$eLast author
000143809 773__ $$0PERI:(DE-600)2001966-X$$a10.1016/j.immuni.2019.03.005$$gVol. 50, no. 5, p. 1218 - 1231.e5$$n5$$p1218 - 1231.e5$$tImmunity$$v50$$x1074-7613$$y2019
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