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pyrimidine nucleotide starvation induces a decrease in the number of effector T cells but not memory T cells

Cellular & Molecular Immunology 2023年第8期20卷 859-860页

作者： Gwanghun Kim hyun Mu Shin Hang-Rae Kim Department of Biomedical Sciences Seoul National University College of MedicineSeoul03080Republic of Korea Department of Anatomy&Cell Biology Seoul National University College of MedicineSeoul03080Republic of Korea BK21 FOUR Biomedical Science project Department of Anatomy&Cell BiologySeoul National University College of MedicineSeoul03080Republic of Korea Medical Research Institute Seoul National University College of MedicineSeoul03080Republic of Korea Wide River Institute of Immunology Seoul National UniversityHongcheon25159Republic of Korea

Scherer et *** the influence of de novo pyrimidine nucleotide synthesis on T-cell responses after antigen stimulation,particularly on effector and memory T-cell development[1].Their work focused on the effect of leflunomide(trade name Avara®),which is a direct inhibitor of dihydroorotate dehydrogenase(DHODH;a key enzyme in the de novo pyrimidine nucleotide pathway and located on the inner mitochondrial membrane).In this pathway,DHODH converts dihydroorotate to orotate and has been implicated in the reduction of ubiquinol to ubiquinone mediated by Complex III in the electron transport *** metabolic effects of DHODH inhibition are unclear[2,3].However,it is known to block S-phase progression by activating *** was originally approved for the treatment of rheumatoid arthritis(RA)in 1998;the mechanism involves the induction of S-phase cell cycle arrest and apoptosis,inhibiting cell proliferation and *** studies have demonstrated the therapeutic potential of leflunomide for cancer[4].Despite the efficacy of leflunomide,the mechanism by which it targets immune cells in the treatment of RA was unknown;however,the work of Scherer and colleagues has shed new light on this mechanism.

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