Regulatory T cells (Tregs) are a suppressive CD4+ T-cell population that help maintain immune tolerance, but in disease they can be co-opted to dampen anti-tumor or inflammatory responses. In glioblastoma multiforme (GBM), they are recruited as part of the tumor’s immunosuppressive resistance program, and the provided key fact notes that GBM recruits Tregs to support immunosuppression. They are also enriched in immunosuppressive niches during PARP inhibitor resistance, and in high-risk bladder cancer both circulating and intratumoral Treg populations are increased as part of an immunosuppressive phenotype. Beyond cancer, a psoriasis mouse model showed that treatment can rebalance the Treg response, indicating a role in inflammatory skin disease and immune homeostasis.
Cancer
- GBM recruits glioblastoma multiforme-associated Tregs to reinforce an immunosuppressive microenvironment and resistance state. (PMID:41720042)
- A 2026 Journal of Clinical Investigation study found Tregs enriched in immunosuppressive niches during PARP inhibitor resistance, linking them to therapy escape. (PMID:41734034)
- In high-risk bladder cancer, circulating and intratumoral Treg populations were increased and associated with an immunosuppressive phenotype. (PMID:42018002)
- The bladder cancer study also connected this phenotype to CD39/CD73-mediated immunosuppression and tumor aggressiveness. (PMID:42018002)
Inflammation / Autoimmunity
- In a psoriasis mouse model, treatment rebalanced the Treg response, suggesting modulation of regulatory immunity can improve disease control. (PMID:41690121)
- The Biomaterials paper on topical ionic liquid-mediated GLUT1 gene editing reported amelioration of psoriasis and prevention of recurrence, with Treg response rebalancing as part of the effect. (PMID:41690121)