LUCAT1/PTBP1/HIF-1α feedback loop promotes T cell over-differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolism.
2/5 보강
PICO 자동 추출 (휴리스틱, conf 2/4)
유사 논문P · Population 대상 환자/모집단
환자: post-traumatic sepsis was examined for LUCAT1, PTBP1, and HIF1A expression
I · Intervention 중재 / 시술
추출되지 않음
C · Comparison 대조 / 비교
추출되지 않음
O · Outcome 결과 / 결론
2-DG partially reversed the effects of LUCAT1 overexpression, whereas HIF1A overexpression countered (rescued) the effects of LUCAT1 silencing. [CONCLUSION] LUCAT1/PTBP1/HIF-1α positive feedback loop drives excessive T cell differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolic reprogramming, which may contribute to disease progression.
OpenAlex 토픽 ·
Cancer, Hypoxia, and Metabolism
Immune Response and Inflammation
Cancer-related molecular mechanisms research
[BACKGROUND] Sepsis, a life-threatening clinical syndrome linked to Th1/Th2-skewed immune imbalance, involves glucose metabolism reprogramming.
APA
Weiyin Gao, Hong Zhang, et al. (2026). LUCAT1/PTBP1/HIF-1α feedback loop promotes T cell over-differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolism.. Cytokine, 203, 157157. https://doi.org/10.1016/j.cyto.2026.157157
MLA
Weiyin Gao, et al.. "LUCAT1/PTBP1/HIF-1α feedback loop promotes T cell over-differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolism.." Cytokine, vol. 203, 2026, pp. 157157.
PMID
42019257
Abstract
[BACKGROUND] Sepsis, a life-threatening clinical syndrome linked to Th1/Th2-skewed immune imbalance, involves glucose metabolism reprogramming. Because women remain under-represented in many sepsis studies and sex-specific host responses may influence disease trajectories, this study aims to delineate the mechanism of lncRNA LUCAT1 in Th1/Th2-skewed immune imbalance during sepsis in women via glucose metabolism reprogramming.
[METHOD] Peripheral blood from female patients with post-traumatic sepsis was examined for LUCAT1, PTBP1, and HIF1A expression. Flow cytometry quantified CD4/CD8 and Th1/Th2 ratios. Starbase analysis predicted regulatory relationships among LUCAT1, PTBP1, and HIF1A. These predictions were validated through dual luciferase reporter gene assays, ChIP, RIP, and actinomycin D assay. Primary human CD4 T cells were cultured and activated with anti-CD3/CD28 (αCD3/CD28), treated with 2-DG (glycolysis inhibitor), and assayed for inflammatory factors (IL-1β, IL-6 and TNF-α), glycolytic genes (GLUT1, HK2, LDHA), glycolytic indexes (glucose uptake, lactate generation, ATP, ECAR and OCR) and Th1/Th2 differentiation.
[RESULT] Post-traumatic sepsis patients display elevated LUCAT1, PTBP1, and HIF1-A in peripheral blood lymphocytes alongside decreased CD4/CD8 and elevated Th1/Th2. HIF-1α promoted LUCAT1 transcription. LUCAT1, acting as a scaffold, may facilitate PTBP1's regulation on HIF1A mRNA stability. Silencing LUCAT1 inhibited and overexpressing LUCAT1 increased inflammatory mediator secretions, glycolysis, Th1/Th2 ratio in αCD3/CD28-induced Primary human CD4 T cells. 2-DG partially reversed the effects of LUCAT1 overexpression, whereas HIF1A overexpression countered (rescued) the effects of LUCAT1 silencing.
[CONCLUSION] LUCAT1/PTBP1/HIF-1α positive feedback loop drives excessive T cell differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolic reprogramming, which may contribute to disease progression.
[METHOD] Peripheral blood from female patients with post-traumatic sepsis was examined for LUCAT1, PTBP1, and HIF1A expression. Flow cytometry quantified CD4/CD8 and Th1/Th2 ratios. Starbase analysis predicted regulatory relationships among LUCAT1, PTBP1, and HIF1A. These predictions were validated through dual luciferase reporter gene assays, ChIP, RIP, and actinomycin D assay. Primary human CD4 T cells were cultured and activated with anti-CD3/CD28 (αCD3/CD28), treated with 2-DG (glycolysis inhibitor), and assayed for inflammatory factors (IL-1β, IL-6 and TNF-α), glycolytic genes (GLUT1, HK2, LDHA), glycolytic indexes (glucose uptake, lactate generation, ATP, ECAR and OCR) and Th1/Th2 differentiation.
[RESULT] Post-traumatic sepsis patients display elevated LUCAT1, PTBP1, and HIF1-A in peripheral blood lymphocytes alongside decreased CD4/CD8 and elevated Th1/Th2. HIF-1α promoted LUCAT1 transcription. LUCAT1, acting as a scaffold, may facilitate PTBP1's regulation on HIF1A mRNA stability. Silencing LUCAT1 inhibited and overexpressing LUCAT1 increased inflammatory mediator secretions, glycolysis, Th1/Th2 ratio in αCD3/CD28-induced Primary human CD4 T cells. 2-DG partially reversed the effects of LUCAT1 overexpression, whereas HIF1A overexpression countered (rescued) the effects of LUCAT1 silencing.
[CONCLUSION] LUCAT1/PTBP1/HIF-1α positive feedback loop drives excessive T cell differentiation and Th1/Th2-skewed immune imbalance in sepsis via glucose metabolic reprogramming, which may contribute to disease progression.
같은 제1저자의 인용 많은 논문 (5)
- Targeting mesenchymal monocyte-derived macrophages to enhance the sensitivity of glioblastoma to temozolomide by inhibiting TNF/CELSR2/p65/Kla-HDAC1/EPAS1 axis.
- Implantable venous access port placement in the upper arm of breast cancer patients with persistent left superior vena cava: a case series and literature review.
- Letter to the editor regarding: Lai, Jimmy Che-To, et al "Non-invasive risk-based surveillance of hepatocellular carcinoma in patients with metabolic dysfunction-associated steatotic liver disease".
- Generating vasculature and immune cell-chimeric tumoroids via intraperitoneal Xenograft.
- ATAD2 drives immunotherapy resistance by promoting lactic acid-mediated CD8 T cell dysfunction in lung adenocarcinoma.