ArticleFrontiers in immunology2022
Bcl-3 regulates the function of Th17 cells through raptor mediated glycolysis metabolism.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Antigenic stimulation in conjunction with cytokine is required for mediating IL-17A production in human MAIT cells.Scientific reports · 2026Article
- T cell fate regulation in EBV‑associated nasopharyngeal carcinoma (Review).Oncology reports · 2026Review
- Antigenic stimulation in conjunction with cytokine is required for mediating IL-17A production in human MAIT cells.bioRxiv : the preprint server for biology · 2026Article
- Interaction networks of macrophage glycolysis and inflammation in sepsis: mechanisms and therapeutic potential.Frontiers in immunology · 2026Review
- Direct-in-NOD genetic ablation of Bcl3 leads to complete type 1 diabetes protection.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Regulation and Function of the Atypical IκBs-Bcl-3, IκBEuropean journal of immunology · 2025Review
- The effect of lactate dehydrogenase inhibitors on proliferation, motility and invasion of breast cancer cellsMolecular medicine reports · 2024Article
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Authors and funding
9 authors.
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Abstract
Bcl-3 is an atypical IκB family member that regulates transcription in the nucleus by binding to the p50/p52 homologous dimer subunit. Although various studies illustrate the important role of Bcl-3 in physiological function, its role in metabolism is still unclear. We found that Bcl-3 has a metabolic regulatory effect on autoimmunity. Bcl-3-depleted mice are unable to develop experimental autoimmune encephalomyelitis. The disease resistance was linked to an increase in lactate levels in Th17 cells, and lactate could alleviate EAE development in WT mice. Bcl-3 deficient mice had more differentiated Th17 cells and an increased extracellular acidification rate in these cells. Concurrently, their ultimate respiration rate and respiratory reserve capacity were significantly lower than wild-type mice. However, adding GNE-140 (LADH inhibitor) to Bcl-3-deficient Th17 cells could reverse the phenomenon, and lactate supplementation could increase the glycolysis metabolism of Th17 cells in WT mice. Mechanically, Bcl-3 could interact with Raptor through ANK and RNC domains. Therefore, Bcl-3 regulates Th17 pathogenicity by promoting Raptor mediated energy metabolism, revealing a novel regulation of adaptive immunity.
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