A clinico-therapeutic analysis

Extensive evidence has confirmed that specific ferroptosis-related metabolic signals or byproducts were involved in the function, viability, and differentiation of multiple T-cell subgroups, impacting their reactivity to inflammation, infection and tumor immunity ( As was reported recently in tumor immunity, the ferroptotic interaction between CD8+ T cell-secreted IFN- and tumor cells is known to induce the elicitation of tumor ferroptosis and reinforcement of anti-tumor activity ( Besides, regulatory T (Treg) cells with a deletion of PDK1 have been implicated in the generation of excessive ROS, which consequently leads to amplified ferroptosis of themselves ( In vitro study corroborated that the suppression of the ROS/TXNIP/HIF-1 pathway, which was presumably associated with the mitochondrial dysfunction in ferroptosis, fosters the ratio of retina-specific Treg cells, notably attenuating ocular inflammation and optic disc edema ( Certain regulators of ferroptosis have emerged as vital contributors in the disruption of the proliferation and survival of CD4+ T cells that potentially exacerbate both tumor progression and pathogen invasion (59, 60)

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