A new mechanism for immune system "brake" molecular regulation was discovered

November 30, 2018 Source: Science and Technology Daily Author: Wang

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In the early morning of November 29th, Beijing time, the international top academic journal Nature, published the research results of Xu Yuqi's research team of the State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Chinese Academy of Sciences. This research reveals for the first time the degradation mechanism of PD-1, a "brake" molecule in the human immune system, and its function in tumor immune response.

As part of the body's immune system, T cells can eliminate mutant cells in the body and prevent tumors from occurring. However, some tumor cells activate the PD-1 molecule to "brake" the immune system, avoiding the killing of T cells, leading to the development of tumors. Clinically, antibody drugs that block the PD-1 pathway can restore the patient's own anti-tumor immune function and achieve the purpose of treating tumors. However, why PD-1 is so "active" in the tumor microenvironment has plagued scientists.

The Xu Yiqi team has been working on the regulation of T cell function. They found that PD-1 has a rapid degradation process in normal T cells, which plays a key role in the protein molecule FBXO38. FBXO38 can add a label that mediates degradation to PD-1. PD-1 with degradation label will be sent to the recovery field of the cell, the proteasome, to ensure that PD-1 maintains normal levels. Affect the function of T cell function. However, in T cells "surrounded" by tumors, FBXO38 is "active" to a low level, which may result in PD-1 not being normally degraded, and T cells are therefore "trapped" by PD-1, which should be degraded. The tumor immune response is inhibited.

The study sheds light on the new regulatory mechanisms of PD-1, an important drug target, which helps researchers better understand tumor immune responses and design new methods for tumor immunotherapy.

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