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Molecular landscape of CD8+ T cells in pure red cell aplasia
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Molecular landscape of CD8+ T cells in pure red cell aplasia
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Journal Article
Molecular landscape of CD8+ T cells in pure red cell aplasia
2025
Overview
The aberrant function of lymphocytes is considered a significant contributing factor to pure red cell aplasia (PRCA), but the precise mechanism by which T lymphocytes induce erythroid development stagnation remains unclear. In our study, the CD8
+
T lymphocytes were isolated from bone marrow aspirates of acquired PRCA patients and healthy controls. RNA sequencing (RNA-Seq) was performed to analyze gene expression profiles. Additionally, the expression levels of key molecules and transcription factors were assessed at the transcription and protein levels. The RNA-Seq analysis revealed a significant upregulation of genes associated with the PI3K/AKT/mTOR pathway in CD8
+
T lymphocytes from patients with PRCA, compared to healthy controls. The mRNA expression of
AKT
,
mTOR
and key transcription factors
T-bet
were significantly upregulated in CD8
+
T cells from patients with PRCA. Treatment with rapamycin, an mTOR inhibitor, attenuated the activation of CD8
+
T lymphocytes in PRCA patients. Our findings demonstrate the activation of the PI3K/AKT/mTOR signaling pathway in CD8
+
T lymphocytes of PRCA patients, suggesting its involvement in PRCA pathogenesis. Targeting this pathway may offer a potential therapeutic strategy for PRCA characterized by CD8
+
T cell dysregulation.
Publisher
Springer Berlin Heidelberg,Springer Nature B.V
Subject
/ Aged
/ CD8-Positive T-Lymphocytes - metabolism
/ CD8-Positive T-Lymphocytes - pathology
/ Female
/ Humans
/ Male
/ Medicine
/ Oncology
/ Phosphatidylinositol 3-Kinases - genetics
/ Phosphatidylinositol 3-Kinases - metabolism
/ Proto-Oncogene Proteins c-akt - genetics
/ Proto-Oncogene Proteins c-akt - metabolism
/ Red-Cell Aplasia, Pure - genetics
/ Red-Cell Aplasia, Pure - immunology
/ Red-Cell Aplasia, Pure - metabolism
/ Red-Cell Aplasia, Pure - pathology
/ Signal Transduction - drug effects
/ TOR Serine-Threonine Kinases - genetics
