Izimila ze-T-cell ezikhulile, njenge-non-Hodgkin T-cell lymphoma, zihlasela kakhulu futhi azikwazi ukumelana nezidakamizwa, futhi iziguli zivame ukuba nokubikezela okubi. Muva nje, uchungechunge lwezihloko ezimbili ze-“Nature” lushicilele incazelo entsha ye-pathogenesis ye-non-Hodgkin's T-cell lymphoma, ngaleyo ndlela inikeze isiqondiso esisha sokuthuthukiswa okuphumelelayo kwezindlela zokwelapha ezintsha zalolu hlobo lwe-lymphoma eyingozi.
In the first study, the Wartewig team used the fusion protein ITK-SYK to construct a transgenic mouse model of late-onset T-cell lymphoma (Nature. Doi: 10.1038 / nature24649), and found that the single or double copy of the PDCD1 gene encoding the PD1 protein was deleted. T cell lymphoma undergoes rapid malignant transformation and accelerates the death of the mouse model. In addition, the application of PD1 or PD-L1 inhibitors can produce similar effects. The related mechanism is that PD1 up-regulates PTEN expression and inhibits the tumor malignant proliferation pathway PI3K.
In another article, Maciocia et al. Applied chimeric antigen receptor T cell immunotherapy (CAR-T) therapy (Nat Med. Doi: 10.1038 / nm.4444) to construct CAR-T cells that specifically target TRBC1 but not TRBC2 To treat TRBC1-positive T-cell carcinoma. While killing tumor cells, leaving enough T cells to fight infection. The clinical trial of this method will be officially launched in 2018.
Umhleli omkhulu wezemvelo u-Megan Cully uthe okutholakele okubalulekile okukhulunywe ngenhla kunikeza isu elisha lokwelashwa lokwelapha izifo ezibulalayo ze-T-cell ezivuthiwe futhi zixwayise ngokuthi lezi zicubu azifaneleki ukwelashwa nge-PD1 noma i-PDL1 inhibitors.
