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Acquired aplastic anemia (AA) is an immune- mediated bone marrow failure syndrome caused by the destruction of hematopoietic stem/progenitor cells (HSPC) by cytotoxic T cells.
Acquired aplastic anemia (AA) is an immune- mediated bone marrow failure syndrome caused by the destruction of hematopoietic stem/progenitor cells (HSPC) by cytotoxic T cells.
immunity
The main feature of immune-mediated AA is the clonal changes of HSPCs: X chromosome inactivation deviation, cytogenetic abnormality, uniparental diploidy of 6p chromosome, paroxysmal nocturnal hemoglobinuria caused by mutation of PIG-A gene in somatic cells Disease and somatic mutations in clonal hematopoietic (CH)-related genes.
Previous studies have shown that oligoclonal CD8+ T cells can often be detected in AA patients, which can induce the apoptosis of homologous HSPC cells.
In addition, the abnormally active T cells in AA patients are closely related to the occurrence and development of the disease, but its antigenic target in HSPC cells is still unknown.
In this study, the researchers sequenced the CD4+ and CD8+ T cells of 24 AA patients, and compared the sequencing results with the whole exome sequencing results of 20 healthy controls and 37 AA patients.
, Designed to analyze the mutations of 2533 genes in T cells of AA patients.
It aims to analyze the mutations of 2533 genes in T cells of AA patients.
JAK-STAT pathway gene mutations in CD4+ or CD8+ T cells in AA patients
JAK-STAT pathway gene mutations in CD4+ or CD8+ T cells in AA patientsTo further understand the impact of the mutation, the researchers performed single-cell sequencing of AA patients with mutations in STAT3 or other genes in CD8+ T cells.
The results showed that the STAT3 mutant clone has cytotoxicity, which can be clearly distinguished from other CD8+ T cells, and the cytotoxicity can be weakened by successful immunosuppressive therapy.
All in all, the results of the study revealed that somatic mutations in T cells are more common and are related to the clonality of cells, and can change the phenotype of T cells.
Therefore, it is necessary to further study its role in the pathogenesis of AA.
org/10.
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