Targeting regulatory T cells in gastric cancer: Pathogenesis, immunotherapy, and prognosis - 13/01/23
Abstract |
Gastric cancer (GC) remains one of the most common malignancies worldwide. Despite immune-checkpoint inhibitors (ICIs) has revolutionized cancer treatment and obtained durable clinical responses, only a fraction of GC patients benefit from it. As an important component of T cells, regulatory T cells (Tregs) play a vital role in the pathogenesis of GC, keep a core balance between immune suppression and autoimmunity, and function as predictive biomarkers for prognosis of GC patients. In this review, we discuss the role of Tregs in the pathogenesis of GC, and targeting Tregs via influencing their transcription factor, migration, co-stimulatory receptors, immune checkpoints, and cytokines. We also focus on the currently important findings of Tregs metabolism including amino acid, fatty acid, and lactic acid metabolism of GC. The emerging role of microbiome and clinical combined therapy in modulating Tregs in GC treatment is also summarized. Meanwhile, this review recapitulates a novel regulator, magnesium, is involved in mediating Tregs in GC. These research advances on Treg-related strategies provide new insights and challenges for GC progression, treatment, and prognosis. And we hope our review can stimulate further discovery and implication of mediators and pathways targeting Tregs.
Le texte complet de cet article est disponible en PDF.Graphical Abstract |
Highlights |
• | Tregs are the major inhibitor cells that exert immune suppression effect in the TME. |
• | Tregs participate in the pathogenesis, immunotherapy, and prognosis of GC. |
• | Targeting the transcription factor, migration, co-stimulatory receptors, immune checkpoints, and cytokines of Tregsin GC. |
• | Tregs in GC can be modulated by the metabolic processes, microbiome, magnesium, and clinical combined therapy. |
Abbreviations : GC, ICI, Tregs, FOXP3, IPEX, nTregs, iTregs, NF-κB, TME, TGF-β, APC, MHCII, TILs, CTL, ATP, ADP, cAMP, ADCC, ADCP, LAG3, DCs, H. pylori, ICOS, ICOS-L, pDCs, TNF, LncRNAs, COX2, PGE2, 15-PGDH, TCF, NF-α, TNFR2, HPD, eTregs, Th, TCR, OA, GCMSCs, p-, GARP, IDO, AHR, TCDD, FFA, FAS, LA, NAD, TCA, PEP, MCT1, C. albicans, MyD88, TLR, MIDAS, MgIG, VEGFR2, OR, ORR, PFS, m6A, m5C
Keywords : Tregs, Co-stimulatory receptors, ICIs, Metabolism, Microbiome, Cytokines, GC
Plan
Vol 158
Article 114180- février 2023 Retour au numéro
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