Recently, a study completed by Dr. Chi Hongbo from the St. Jude Children's Research Hospital in the United States revealed a LKB1 signaling pathway closely related to the activation of regulatory T cell function. The study's corresponding article was published in the latest issue of Nature, entitled "Homeostatic control of metabolic and functional fitness of Treg cells by LKB1 signalling."

Hepatocyte kinase B1 (LKB1) is one of the important tumor suppressor proteins and is essential for the control of tumor cell growth and metabolic processes. Based on studies in mouse models, the researchers found that LKB1 dysfunction in regulatory T cells severely disrupts the normal metabolism and function of regulatory T cells, leading to the development of regulatory T cells, which in turn causes mice to develop. Extremely severe inflammatory response.

"We know that regulatory T cells have both dormancy and activation," Dr. Chi Hongbo said. "Our results suggest that when the LKB1 signaling pathway in regulatory T cells is inactivated, the normal function of regulatory T cells is also It will be lost. Regulatory T cell failure is closely related to a variety of autoimmune diseases. This study proposes a potential novel autoimmune disease treatment that enhances regulatory T cells by regulating cellular metabolism. Function to treat related autoimmune diseases."

In addition to the above results, the study also highlighted the important role of metabolism in normal immune function. The loss of LKB1 signaling pathway in regulatory T cells also destroys the normal metabolism of various substances in mitochondria to some extent, and has many negative effects on the energy response in the mitochondria.

"The LKB1 pathway links the cellular immune system with the material energy metabolism system, especially the cellular metabolic system associated with mitochondrial function," said Dr. Kai Yang, the lead author of the article.

During the course of the study, Dr. Chi and his colleagues also found that regulatory T cells deficient in the LKB1 pathway were able to express more PD-1 molecules than normal regulatory T cells, and that elevated PD-1 molecules were involved in regulatory T. The immune function of the cells was further activated, which enhanced the immune function of the mice to some extent. By inhibiting PD-1, the activity and function of regulatory T cells in mice are significantly restored, and the activated immune function is also inhibited at the original level. To some extent, this accidental and important discovery provides new ideas and methods for immunotherapy of cancer.

"Our data strongly suggests that the regulation of regulatory T cell failure plays an important role in the development of autoimmune diseases. By regulating the metabolism of regulatory T cells, we are expected to develop new methods for the treatment of autoimmune diseases." Dr. Chi Hongbo added .

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