Increased HIF-1α expression in T cells and associated with enhanced Th17 pathway in systemic lupus erythematosus
In: Journal of the Formosan Medical Association, Jg. 121 (2022), Heft 12, S. 2446-2456
Online
academicJournal
Zugriff:
Background/Purpose: Recent emerging evidence indicates that dysfunction of metabolic remodeling underlies aberrant T cell immune responses in systemic lupus erythematosus (SLE). This study was undertaken to investigate the expression of HIF-1α, a regulator of metabolic reprogramming, in T cells from SLE. Methods: HIF-1α expression in T lymphocytes from SLE patients was examined by quantitative polymerase chain reaction (PCR) and the protein expression was analyzed with intracellular staining in flow cytometry. HIF-1α was overexpressed in murine CD4 T cells via transducing T cells with HIF-1α containing lentivirus. The expression of HIF-1α, metabolic- and Th17-associated genes in T cells from SLE patients and its association with clinical manifestation was analyzed. Results: HIF-1α expression is increased in CD4 T cells from SLE patients both in intracellular staining and quantitative PCR analysis. In addition, there is enhanced HIF-1α expression in Th17-skewing murine T cells, and lentivirus-mediated HIF-1α overexpression promotes Th17 differentiation. Moreover, HIF-1α gene expression is positively correlated with the expression of glycolysis- and IL-17-associated genes in SLE patients. Conclusion: HIF-1α expression is increased in T cells from SLE patients, and is positively correlated with glycolysis- and Th17- associated pathway, implicating HIF-1α contributes to the activation of Th17 cells in SLE, and represents a potential novel therapeutic target.
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Increased HIF-1α expression in T cells and associated with enhanced Th17 pathway in systemic lupus erythematosus
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Autor/in / Beteiligte Person: | Liao, Hsiu-Jung ; Chu, Ching-Liang ; Wang, Szu-Chieh ; Lee, Hua-Yi ; Wu, Chien-Sheng |
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Zeitschrift: | Journal of the Formosan Medical Association, Jg. 121 (2022), Heft 12, S. 2446-2456 |
Veröffentlichung: | Elsevier, 2022 |
Medientyp: | academicJournal |
ISSN: | 0929-6646 (print) |
DOI: | 10.1016/j.jfma.2022.05.003 |
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