The kinetics of mTORC1 activation associates with FOXP3 expression pattern of CD4+ T cells and outcome of steroid-sensitive minimal change disease

Chen, Guochun; Mi, Zeng; Liu, Zhiwen; Zhou, Mingmei; Zha, Jie; Zhang, Lei; Chen, Huihui; Liu, Hong

doi:10.1016/j.intimp.2023.110589

Cited by 2 publications

(1 citation statement)

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“… 9 Notably, the dynamics of FOXP3 expression in CD4 + T cells strongly align with the long‐term results of glucocorticoid therapy in patients suffering from glomerular disease. 10 Furthermore, our latest findings underscore the critical epigenetic regulatory role of long‐term glucocorticoid treatment in the biology of CD4 + T cells. 11 Collectively, current evidence suggests that GCs promote anti‐inflammatory Th2 and Treg responses while suppressing pro‐inflammatory Th1 and Th17 responses.…”

Section: Introductionmentioning

confidence: 80%

Glucocorticoid regulation of the mTORC1 pathway modulates CD4⁺ T cell responses during infection

Chen,

Liu,

Zha

et al. 2023

Clin & Trans Imm

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ObjectivesConventional glucocorticoid (GC) treatment poses significant risks for opportunistic infections due to its suppressive impact on CD4+ T cells. This study aimed to explore the mechanisms by which GCs modulate the functionality of CD4+ T cells during infection.MethodsWe consistently measured FOXP3, inflammatory cytokines and phospho‐S6 ribosomal protein levels in CD4+ T cells from patients undergoing conventional GC treatment. Using Foxp3EGFP animals, we investigated the dynamic activation of the mechanistic target of rapamycin complex 1 (mTORC1) pathway and its correlation with the immunoregulatory function of CD4+ T cells under the influence of GCs.ResultsGCs dynamically altered the expression pattern of FOXP3 in CD4+ T cells, promoting their acquisition of an active T regulatory (Treg) cell phenotype upon stimulation. Mechanistically, GCs undermined the kinetics of the mTORC1 pathway, which was closely correlated with phenotype conversion and functional properties of CD4+ T cells. Dynamic activation of the mTORC1 signaling modified the GC‐dampened immunoregulatory capacity of CD4+ T cells by phenotypically and functionally bolstering the FOXP3+ Treg cells. Interventions targeting the mTORC1 pathway effectively modulated the GC‐dampened immunoregulatory capacity of CD4+ T cells.ConclusionThese findings highlight a novel mTORC1‐mediated mechanism underlying CD4+ T cell immunity in the context of conventional GC treatment.

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Section: Introductionmentioning

confidence: 80%

Glucocorticoid regulation of the mTORC1 pathway modulates CD4⁺ T cell responses during infection

Chen,

Liu,

Zha

et al. 2023

Clin & Trans Imm

Self Cite

View full text Add to dashboard Cite

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Immune landscape in the glomerular transcriptome of nephrotic syndrome and anca-associated vasculitis

Feng,

Yi,

et al. 2024

Acta Clinica Belgica

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The kinetics of mTORC1 activation associates with FOXP3 expression pattern of CD4+ T cells and outcome of steroid-sensitive minimal change disease

Cited by 2 publications

References 49 publications

Glucocorticoid regulation of the mTORC1 pathway modulates CD4⁺ T cell responses during infection

Glucocorticoid regulation of the mTORC1 pathway modulates CD4⁺ T cell responses during infection

Immune landscape in the glomerular transcriptome of nephrotic syndrome and anca-associated vasculitis

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The kinetics of mTORC1 activation associates with FOXP3 expression pattern of CD4+ T cells and outcome of steroid-sensitive minimal change disease

Cited by 2 publications

References 49 publications

Glucocorticoid regulation of the mTORC1 pathway modulates CD4+ T cell responses during infection

Glucocorticoid regulation of the mTORC1 pathway modulates CD4+ T cell responses during infection

Immune landscape in the glomerular transcriptome of nephrotic syndrome and anca-associated vasculitis

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Glucocorticoid regulation of the mTORC1 pathway modulates CD4⁺ T cell responses during infection

Glucocorticoid regulation of the mTORC1 pathway modulates CD4⁺ T cell responses during infection