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Immunity | PD-1抑制性受体下调天冬酰胺内肽酶并维持诱... http://www.360doc.com/content/19/0529/09/52645714_83890...

Immunity | PD-1抑制性受体下调天冬酰胺内肽酶并维持诱导调节性
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生物_医药_科研
Immunity | PD-1抑制性受体下调天冬酰胺内肽酶
并维持诱导调节性T细胞中Foxp3转录因子... 关注 对话

生物_医药_科研 2019-05-29 | 130阅读 | 1转藏


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恒瑞创新药卡瑞利珠单抗联合阿帕替尼…
PD-1 Inhibitory Receptor Downregulates Asparaginyl Endopeptidase and
17 款四代靶向药,全面攻坚 EGFR 耐药
Maintains Foxp3 Transcription Factor Stability in Induced Regulatory T Cells
最全整理汇总:HER2阳性乳腺癌靶向治…

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Immunity 2018
部编人教版一年级道德与法治下册知识
CD4+ T cell differentiation into multiple T helper (Th) cell lineages is critical for 要点复习提纲 阅8734

optimal adaptive immune responses. This report identifies an intrinsic mechanism by 完整的八宅风水断事口诀,八宅风水吉
which programmed death-1 receptor (PD-1) signaling imparted regulatory phenotype 凶方位图解 阅118419

to Foxp3+ Th1 cells (denoted as Tbet+ iTregPDL1 cells) and inducible regulatory T 伤寒论条文398条(全) 阅100621

(iTreg) cells. Tbet+ iTregPDL1 cells prevented inflammation in murine models of 危险化学品事故专项应急预案 阅12575

experimental colitis and experimental graft versus host disease (GvHD). Programmed 项目管理方案和实施方案概述 阅26414
death ligand-1 (PDL-1) binding to PD-1 imparted regulatory function to Tbet+
iTregPDL1 cells and iTreg cells by specifically downregulating endolysosomal protease
asparaginyl endopeptidase (AEP). AEP regulated Foxp3 stability and blocking AEP
imparted regulatory function in Tbet+ iTreg cells. Also, Aep/ iTreg cells significantly
inhibited GvHD and maintained Foxp3 expression. PD-1- mediated Foxp3
maintenance in Tbet+ Th1 cells occurred both in tumor infiltrating lymphocytes (TILs)
and during chronic viral infection. Collectively, this report has identified an intrinsic

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Immunity | PD-1抑制性受体下调天冬酰胺内肽酶并维持诱... http://www.360doc.com/content/19/0529/09/52645714_83890...

function for PD-1 in maintaining Foxp3 through proteolytic pathway. 搜索


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Paracrine Wnt5a-β-catenin Signaling Triggers a Metabolic Program That Drives 这个夏天最值得记录的,对你来说是…

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骨盆评估之坐位体前屈试验

谈古论今(七律)

Fei. Zhao,1 Christine Xiao,1 Kathy S. Evans,1 Tbalamayooran Theivanthiran,1 Nicholas


DeVito,1 Alisha Holtzhausen,1,2 Juan Liu,4 Xiaojing Liu,4 David Boczkowski,3 Smita
Nair,3 Jason W. Locasale,4 and Brent A. Hanks1,§

Immunity 2018

Despite recent advances, many cancers remain refractory to available


immunotherapeutic strategies. Emerging evidence indicates that the tolerization of
local dendritic cells (DCs) within the tumor microenvironment promotes immune
evasion. Here have described a mechanism by which melanomas establish a site of
immune privilege via a paracrine Wnt5a-β-catenin-peroxisome proliferator-activated
receptor-γ (PPAR-γ) signaling pathway that drives fatty acid oxidation (FAO) in DCs by
upregulating the expression of the carnitine palmitoyltransferase-1A (CPT1A) fatty
acid transporter. This FAO shift increased the protoporphyrin IX prosthetic group of
indoleamine 2,3-dioxgenase-1 (IDO) while suppressing interleukin-6 (IL-6) and IL-12
cytokine expression, culminating in enhanced IDO activity and the generation of
regulatory T cells. They demonstrated that blockade of this pathway augmented anti-
melanoma immunity, enhanced the activity of anti-PD-1 antibody immunotherapy,
and suppressed disease progression in a transgenic melanoma model. This work
implicates a role for tumor-mediated metabolic reprogramming of local DCs in
immune evasion and immunotherapy resistance.

Edited by Biaolong Deng

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Immunity | PD-1抑制性受体下调天冬酰胺内肽酶并维持诱... http://www.360doc.com/content/19/0529/09/52645714_83890...

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