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作 者:Amit Sharma Ingo G.H.Schmidt-Wolf
出 处:《Cellular & Molecular Immunology》2023年第12期1401-1402,共2页中国免疫学杂志(英文版)
摘 要:Although cancer immunotherapy has taken center stage,exhaustion of T cells is undeniably one of the major problems preventing it from being fully successful[1].Certainly,reversal of T-cell exhaustion or dysfunction is of great importance for developing new strategies and restoring immune function.Nevertheless,counterarguments about the adverse effect of reversing T-cell exhaustion(leading to overactivation of T cells and cytotoxicity)and even their irreversible properties have been quite common in scientific debates.With more to be discovered about the reasons for T-cell failure,a better understanding of the molecular factors/determinants[2,3]that shape/remodel“heterogeneous”dysfunctional T cells in cancer makes clear sense.Indeed,two recent publications in Nature immunology have described the intriguing perspective of T-cell exhaustion[4,5].Of interest,Vignali et al.focused on the hypoxia-driven CD39-dependent suppressor function of exhausted T cells,whereas Saadey et al.emphasized restoring the epigenetic balance of TGFβ1/BMP signaling in exhausted T cells to unlock responsiveness to immune checkpoint blockade therapy.
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