Transcription regulates HIF-1α expression in CD4+ T cells

Thomas Bollinger*, Annalena Bollinger, Sydney Gies, Lea Feldhoff, Werner Solbach, Jan Rupp

*Corresponding author for this work
2 Citations (Scopus)


The transcription factor hypoxia inducible factor-1α (HIF-1α) mediates the metabolic adaptation of cells to hypoxia and T-helper cell fate. However, HIF-1α regulation in CD4 + T cells (T cells) remains elusive. Here we observed that depletion of oxygen (O 2 ≤2%) alone was not sufficient to induce HIF-1α expression in T cells. However, when hypoxic T cells were stimulated, HIF-1α was expressed and this was dependent on nuclear factor-κB- and nuclear factor of activated T cell (NFAT)-mediated transcriptional upregulation of Hif-1α mRNA. HIF-1α upregulation could be blocked by drugs inhibiting NF-κB, NFAT or mammalian target of rapamycin precluding CD4 + T-cell stimulation or translation in T cells, as well as by blocking transcription. CD3, CD28, phorbol-12-myristat-13-acetat (PMA) or ionomycin-stimulated T cells did not express HIF-1α under normoxic conditions. In conclusion, regulation of HIF-1α expression in CD4 + T cells in hypoxia gravely relies on its transcriptional upregulation and subsequent enhanced protein stabilization.

Original languageEnglish
JournalImmunology and Cell Biology
Issue number1
Pages (from-to)109-113
Number of pages5
Publication statusPublished - 01.01.2016

Research Areas and Centers

  • Academic Focus: Center for Infection and Inflammation Research (ZIEL)


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