A joint research team from CNU and Seoul National University discovered a mechanism for regulating the homeostasis of new CD8 T-cells linked to interferon signaling.

The research team led by CNU Professor Cho Jae-ho (Department of MRC of the College of Medicine) confirmed that the STAT1 protein, an interferon signal tranx-x-scription factor, acts as a homeostatic regulator of new CD8 T-cells in a normal, uninfected, living environment through a joint study with Professor Yoon Cheol-hee's team at Seoul National University.

The research team discovered abnormally activated CD8 T-cells in a mutant mouse model lacking the STAT1 gene and applied various molecular biological experimental techniques to investigate the mechanism of abnormal interferon signaling in STAT1-deficient neonatal CD8 T-cells.

This highlights the importance of the interferon signaling system as a homeostasis factor, which is different from its role as an existing antiviral factor.

STAT1, an interferon signal tranx-x-scription factor, is known as an important factor in various immune-related diseases such as pathogen infection, autoimmune diseases, and cancer, and polymorphisms and mutations in the human STAT1 gene have also been reported.

Professor Cho said, “This study can contribute to improving the understanding of diseases caused by interferon signaling abnormalities. In the future, research on new interferon signaling modulators and activators will be accelerated in the field of immunotherapeutics targeting CD8 T-cells.”

This research was conducted with support from the Ministry of Science and ICT, the Ministry of Health and Welfare, and the National Research Foundation's Basic Research Project and Source Technology Development Project. The results of this study were published in the online edition of Science Advances (impact factor 14.136), an international scientific journal on September 1.