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Fig. 2 | Cancer Cell International

Fig. 2

From: Membrane protein trafficking in the anti-tumor immune response: work of endosomal-lysosomal system

Fig. 2

The endocytosis, trafficking and degradation of immune checkpoint PD-L1 and B7(CD80/86) on the tumor cell and PD-1 and CTLA-4 on the lymphocyte. ICs are transcribed and translated in the endoplasmic reticulum, modified in the Golgi apparatus, and vesicles are transported to the plasma membrane, where ICs interaction with the ligand. Some vital regulator controls the endocytosis, recycling and degradation of ICs. CMTM-family proteins promote the recycling of PD-L1 back to the plasma membrane and inhibits the lysosomal degradation of PD-L1; HIP1R mediates the lysosomal degradation of PD-L1; And DHHC3 palmitoylates the PD-L1 promoting the lysosomal degradation of PD-L1. The expression of the March-I down-regulating CD86. Rab11 and PD-1 co-locate in the recycle endosomes. DHHC9 palmitoylates the PD-1 promoting the lysosomal degradation of PD-1; On the contrary, TOX binds with PD-1 in the cytoplasm and facilitating PD-1 recycling. CTLA-4: Reduction of LRBA promotes the lysosomal degradation of CTLA-4

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