期刊
FEBS JOURNAL
卷 282, 期 14, 页码 2661-2681出版社
WILEY
DOI: 10.1111/febs.13306
关键词
Ca2+ influx; immune activation and effector function; neuro-immune interaction; T cells; T cell receptor; TRPV channels
资金
- Department of Biotechnology, Government of India [BT/PR14128/BRB/10/814/2010, BT/PR13782/PID/06/533/2010, BT/PR13312/GBD/27/247/2009]
- Council of Scientific and Industrial Research, Government of India [37(1542)/12/EMR-II]
- Imaging Facility of NISER
- Flow Cytometry Facility of NISER
The importance of Ca2+ signalling and temperature in the context of T cell activation is well known. However, the molecular identities of key players involved in such critical regulations are still unknown. In this work we explored the endogenous expression of transient receptor potential vanilloid (TRPV) channels, a group of thermosensitive and non-selective cation channels, in T cells. Using flow cytometry and confocal microscopy, we demonstrate that members belonging to the TRPV subfamily are expressed endogenously in the human T cell line Jurkat, in primary human T cells and in primary murine splenic T cells. We also demonstrate that TRPV1- and TRPV4-specific agonists, namely resiniferatoxin and 4 alpha-phorbol-12,13-didecanoate, can cause Ca2+ influx in T cells. Moreover, our results show that expression of these channels can be upregulated in T cells during concanavalin A-driven mitogenic and anti-CD3/CD28 stimulated TCR activation of T cells. By specific blocking of TRPV1 and TRPV4 channels, we found that these TRPV inhibitors may regulate mitogenic and T cell receptor mediated T cell activation and effector cytokine(s) production by suppressing tumour necrosis factor, interleukin-2 and interferon-c release. These results may have broad implications in the context of cell-mediated immunity, especially T cell responses and their regulations, neuro-immune interactions and molecular understanding of channelopathies.
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