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Cytotoxic T lymphocytes (CTLs) are important immune cells that clear pathogens and tumors
.
Following infection, CD8 + T cells differentiate into short-lived effector cells (SLECs; KLRG1 + CD127 - ) or memory precursor effector cells (MPECs; KLRG1 - CD127 + )
On December 3, 2021, the research group of Prof.
Xiao Nengming, School of Life Sciences/State Key Laboratory of Cell Stress Biology, Xiamen University, published a paper entitled "Mitochondrial C1qbp promotes differentiation of effector CD8 + T cells via metabolic- Epigenetic reprogramming" research paper revealed the important regulatory role of mitochondrial C1qbp in effector CD8 + T cell differentiation and its molecular mechanism, providing a mechanistic link between mitochondrial metabolism and effector CD8 +
T cell differentiation .
C1qbp (complement C1q-binding protein, also known as p32 or gC1qR) is a multifunctional protein known to be important for mitochondrial oxidative phosphorylation, which promotes the translation of mitochondrial genes-encoded proteins by binding to RNA
.
The role of C1qbp in T cells is still lacking
The researchers found that C1qbp can be transiently induced after T cell activation; in an experimental model of LCMV virus acute infection and a B16F10 melanoma model, T cell-specific C1qbp knockout ( C1qbp fl /fl dLckCre) mice CD8 + T cells could not normally differentiate into short-lived effector T cells, and the ability to secrete effector cytokines was also significantly reduced
.
In activated C1qbp-deficient CD8 + T cells, mitochondrial morphology changed significantly, protein synthesis of respiratory chain subunit encoded by mitochondrial genes was inhibited, mitochondrial functions such as oxidative phosphorylation and mitochondrial membrane potential that should have been rapidly enhanced were impaired, and metabolic pathways were disordered ; led to a significant increase in the content of 2-hydroxyglutaric acid (2-HG) and fumarate (Fumarate), while the level of acetyl-CoA was significantly decreased
To further confirm whether the altered metabolites affect effector cell differentiation, the researchers treated wild-type CD8 + T cells with fumarate, which significantly inhibited the differentiation of effector CD8 + T cells, making them more inclined to form memory precursor cells , and the ability of CD8 + T cells to secrete effector cytokines was significantly inhibited, which partly mimics the effector T cell differentiation-deficient phenotype of C1qbp-deficient CD8 +
T cells .
Concurrent treatment of cells with a histone deacetylase inhibitor (tubastatin A) and acetate significantly compensated for the deficiency of C1qbp-deficient CD8 + T cells to differentiate into effector cells and secrete effector cytokines
This study is the first to report that mitochondrial C1qbp can promote effector CD8 + T cell differentiation through metabolic-epireprogramming, highlighting the critical role of mitochondria in CD8 + T cell differentiation and function, and pointing out that metabolic intervention may improve T cells in diseases such as cancer Cell therapy effect
.
Our doctoral students Zhai Xingyuan, Liu Kai and medical school doctoral student Fang Hongkun are the co-first authors of the paper
.
Professor Xiao Nengming from the School of Life Sciences and Professor Li Qiyuan from the School of Medicine are the co-corresponding authors of this paper
Professor Xiao Nengming is committed to the research of anti-virus and anti-tumor T-cell immunity, and has been published in important academic journals such as Nature Immunology , Science Advances , Blood , PNAS , J Immunol , Front Immunol as the (co) first author or (co) corresponding author .
Published several research papers
.
The research group plans to recruit postdoctoral fellows and recruit several doctoral and master students to join the team to carry out tumor immune research.
Full text link: https:// Xiao Nengming's research group)
