One of the most common promoters of the initiation and growth of the tumor is an immune disturbance. Numerous immune cells and inflammatory factors play a role in the tumor‐immune microenvironment. However, few studies have investigated the correlation between these immunological events and clinical consequences in cervical cancer. We measured the levels of numerous inflammatory mediators and frequencies of regulatory T cells (Tregs), myeloid‐derived suppressor cells (MDSCs) and mucosal‐associated invariant T (MAIT) cells in peripheral blood (PB) of cervical cancer patients. Cervical cancer patients showed elevated production of interleukin (IL)‐18 and plasma C‐C chemokine ligand (CCL) 3/5. Meanwhile, an accumulation of C‐C chemokine receptor 5 (CCR5) monocytic (Mo)‐MDSCs and Tregs was observed. The cervical cancer group displayed increased frequencies of CD8+, CD4+ and highly activated CD38+CD8+MAIT cells, and reduction of double‐negative (DN) and PD1(CD279+) DN MAIT cells. Importantly, it was demonstrated that MAIT cells were positively related to Mo‐MDSCs. Furthermore, an elevated concentration of PD1(CD279+) DN MAIT cells was significantly related to increased progression‐free survival of patients with cervical cancer. In conclusion, our study suggests that the combined action of Mo‐MDSCs and MAIT cells might be associated with the progression of cervical cancer, and the frequency of DN MAIT cells in the peripheral blood mononuclear cells was associated with the survival benefit of patients.
The mitochondrial DNA (mtDNA) m.3243A>G mutation is one of the most common pathogenic mtDNA variants, showing complex genetics, pathogenic molecular mechanisms, and phenotypes. In recent years, the prevention of mtDNA-related diseases has trended toward precision medicine strategies, such as preimplantation genetic diagnosis (PGD) and mitochondrial replacement therapy (MRT). These techniques are set to allow the birth of healthy children, but clinical implementation relies on thorough insights into mtDNA genetics. The genotype and phenotype of m.3243A>G vary greatly from mother to offspring, which compromises genetic counseling for the disease. This review is the first to systematically elaborate on the characteristics of the m.3243A>G mutation, from genetics to phenotype and the relationship between them, as well as the related influencing factors and potential strategies for preventing disease. These perceptions will provide clarity for clinicians providing genetic counseling to m.3243A>G patients.
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