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Behets syndrome as a model of thrombo-inflammation: the role of neutrophils

Its core molecular mechanisms involve the collapse of the antioxidant defense system, particularly the inactivation of glutathione peroxidase 4 (GPX4), inhibition of the cystine/glutamate antiporter (System Xc - ), and dysregulation of the ferroptosis suppressor protein 1 (FSP1) pathway ( - supports GPX4 function by maintaining the supply of cysteine and GSH, whereas FSP1 independently inhibits lipid peroxidation by reducing the level of ubiquinone (CoQ10), thereby preventing ferroptosis ( 2+ , thereby promoting ferroptosis and suppressing tumor growth ( The tumor immune microenvironment (TIME) of GBM is characterized by highly immunosuppressive characteristics, marked by the polarization of tumor-associated macrophages (TAMs) toward the M2 phenotype, T-cell functional exhaustion, excessive infiltration of regulatory T cells (Tregs), and high expression of the immune checkpoint molecules PD1/PD-L1 ( Figure 1 ) The unique TIME of GBM not only promotes tumor cell growth and invasion but also limits the efficacy of existing chemotherapy and radiotherapy ( + T-cell exhaustion and Treg enrichment further constrain cytotoxic T lymphocyte (CTL) activity, impairing antitumor immunity and facilitating immune escape ( Figure 1 Metabolic alterations are considered key drivers in regulating the suppressive TIME of GBM

doi: 10.1016/j.tim.2019.03.008 225 KryczkaJ.BoncelaJ

doi: 10.1016/j.gca.2018.04.016 305 XuL.LiuT.LiuL.YaoX.ChenL.FanD.et al