ArticleJournal of neuroimmunology2011
Vasoactive intestinal peptide receptor 1 is downregulated during expansion of antigen-specific CD8 T cells following primary and secondary Listeria monocytogenes infections.
Article in Journal of neuroimmunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 9 citations in OpenAlex.
- Hypoxia Is a Dominant Remodeler of the Effector T Cell Surface Proteome Relative to Activation and Regulatory T Cell Suppression.Molecular & cellular proteomics : MCP · 2022Article
- The G Protein-Coupled Receptor, VPAC1, Mediates Vasoactive Intestinal Peptide-Dependent Functional Homeostasis of the Gut Microbiota.Gastro hep advances · 2022Article
- [Expression of vasoactive intestinal peptide in peripheral blood of children with hand, foot and mouth disease].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2016Article
- Illuminating the petite picture of T cell memory responses to Listeria monocytogenes.BioMed research international · 2013Review
- Urokinase plasminogen activator receptor induced non-small cell lung cancer invasion and metastasis requires NHE1 transporter expression and transport activity.Cellular oncology (Dordrecht, Netherlands) · 2012Article
- Vasoactive intestinal peptide signaling axis in human leukemia.World journal of biological chemistry · 2011Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
As regulation of CD8 T cell homeostasis is incompletely understood, we investigated the expression profile of the vasoactive intestinal peptide (VIP) receptors, VPAC1 and VPAC2, on CD8 T cells throughout an in vivo immune response. Herein, we show that adoptively transferred CD8 T cells responding to a Listeria monocytogenes infection significantly downregulated, functionally active VPAC1 protein expression during primary and secondary expansion. VPAC1 mRNA expression was restored during contraction and regained naïve levels in primary, but remained low during secondary, memory generation. VIP co-administration with primary infection suppressed CD8 T cell expansion (≈ 50%). VPAC2 was not detected at any time points throughout primary and secondary infections. Collectively, our data demonstrate that functionally active VPAC1 is dynamically downregulated to render expanding CD8 T cells unresponsive to VIP.
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Registered trials
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