Zreli tumori T-stanica, poput ne-Hodgkinovog limfoma T-stanica, vrlo su invazivni i otporni na lijekove, a pacijenti često imaju lošu prognozu. Nedavno je serija "Nature" iz dva članka objavila novo tumačenje patogeneze ne-Hodgkinovog T-staničnog limfoma, pružajući tako novi smjer za učinkovit razvoj novih terapija za ovu vrstu malignog limfoma.
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.
Viša urednica Nature, Megan Cully, rekla je da gore spomenuti važni nalazi pružaju novu strategiju liječenja zrelih malignih tumora T-stanica i upozoravaju da ti tumori nisu prikladni za liječenje inhibitorima PD1 ili PDL1.
