A Korean research team has raised the possibility of developing vaccines to prevent chronic infectious diseases such as infections, AIDS, tuberculosis and to prevent the recurrence of cancer.
The Korea Health Industry Development Institute한국보건산업진흥원 has collaborated with Professor Ha Sang-joon하상준 of Yonsei University연세대 and Dr. Kim Tae-don김태돈 of the Korea Research Institute of Bioscience and Biotechnology한국생명공학연구원 to demonstrate for the first time that microRNA-150 has a new function in regulating the differentiation of memory T cells.
The Ministry of Health and Welfare복지부 supported the study to develop an anti-infectious disease countermeasure project called "the immunization vaccine development to overcome intractable tuberculosis."
MicroRNA-150 controls the expression of various life phenomena related to development, growth, aging, and immunity in cells, while memory T cells is a lymphocyte that can directly kill infected cells or tumor cells. Memory T cells also memorize pathogens or tumor antigens and induce an intense and rapid immune response when reinfection of pathogens or tumor recurs.
In patients with chronic infection or cancer, the memory T cells do not form properly, which is why it’s necessary to develop a vaccine capable of efficiently inducing memory T cell differentiation, the institution said.
When T cells recognize external antigens, some of them differentiate into memory T cells. When memory T cells are re-exposed to the same antigen, they produce a strong secondary immune response, which inhibits reinfection or tumor recurrence of the pathogen.
To investigate the effect of microRNA-150 on the differentiation of memory T cells, the research team analyzed the T cell differentiation after infecting mice deficient in microRNA-150.
The results of the analysis confirmed that the differentiation of the memory T cells was accelerated compared with that of the normal mice. The T cells lacking microRNA-150 showed an increase in the expression of the Foxo1 protein in the differentiation, T cells overexpressing microRNA-150 have been shown to inhibit Foxo1 protein expression.
Also, mice transplanted with microRNA-150 deficient memory T cells are more likely to be infected with viruses with external antigens that have been exposed compared to mice transplanted with normal memory T cells and to control the proliferation of stronger tumor cells.
"This study has identified the key mechanism of action of microRNA-150 in memory T cell differentiation," Professor Ha said. "It will be an important clue for the development of preventive vaccines and anti-cancer vaccines for infectious diseases such as hepatitis C, AIDS, and tuberculosis."