2019
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Abstract: Objective. Takayasu arteritis (TAK) is a progressive autoimmune large vessel vasculitis with infiltration of proinflammatory T cells, with a largely unknown etiology. This study was undertaken to explore the involvement of mechanistic target of rapamycin (mTOR) in proinflammatory T cell differentiation and disease progression in TAK.Methods. Ninety-five patients with TAK, 26 patients with small vessel vasculitis, and 40 healthy donors were enrolled. Naive and memory CD4+ T cells were activated with anti-CD3/CD… Show more

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“…A shared feature of CD4 + T cells in both GCA and TAK is the strong upregulation of mTORC1 activity (13,14). mTOR is a signaling hub in T cell fate decisions and mTORC1 activation biases T cell differentiation toward the Th1 and Th17 lineage.…”
Section: Cd4 + Effector T Cellmentioning
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“…A shared feature of CD4 + T cells in both GCA and TAK is the strong upregulation of mTORC1 activity (13,14). mTOR is a signaling hub in T cell fate decisions and mTORC1 activation biases T cell differentiation toward the Th1 and Th17 lineage.…”
Section: Cd4 + Effector T Cellmentioning
“…Strong evidence for mTORC1's role as a key decision maker comes from studies using rapamycin to guide T cell differentiation. The mTORC1 blocker was able to prevent differentiation into Th1 and Th17 cells (13,14). The cause of persistent mTORC1 activation in GCA and TAK T cells is not understood but may be an independent factor in directing disease-relevant immunity.…”
Section: Cd4 + Effector T Cellmentioning
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“…I read with interest the report by Zhang et al, describing their study demonstrating that CD4+ T cells isolated from patients with Takayasu arteritis (TAK) are biased to detect the spontaneous differentiation of Th1 and Th17 cells because of hyperactivity of mechanistic target of rapamycin complex 1 (mTORC1) . Subsequently, using human artery–NSG mouse chimeras, they showed that mTORC1 inhibition, by either rapamycin or RNAi technology, effectively abrogated the maldifferentiation of TAK CD4+ T cells and vascular inflammation .…”
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