Fluoxetine suppresses calcium signaling in human T lymphocytes through depletion of intracellular calcium stores

10Citations
Citations of this article
17Readers
Mendeley users who have this article in their library.

Abstract

Selective serotonin reuptake inhibitors, such as fluoxetine, have recently been shown to exert anti-inflammatory and immunosuppressive effects. Although the effects on cytokine secretion, proliferation and viability of T lymphocytes have been extensively characterized, little is known about the mechanism behind these effects. It is well known that Ca2+ signaling is an important step in the signaling transduction pathway following T cell receptor activation. Therefore, we investigated if fluoxetine interferes with Ca2+ signaling in Jurkat T lymphocytes. Fluoxetine was found to suppress Ca2+ signaling in response to T cell receptor activation. Moreover, fluoxetine was found to deplete intracellular Ca2+ stores, thereby leaving less Ca2+ available for release upon IP3- and ryanodine-receptor activation. The Ca2+-modifying effects of fluoxetine are not related to its capability to block the serotonin transporter, as even a large excess of 5HT did not abolish the effects. In conclusion, these data show that fluoxetine decreases IP3- and ryanodine-receptor mediated Ca2+ release in Jurkat T lymphocytes, an effect likely to be at the basis of the observed immunosuppression.

Cite

CITATION STYLE

APA

Gobin, V., De Bock, M., Broeckx, B. J. G., Kiselinova, M., De Spiegelaere, W., Vandekerckhove, L., … Deforce, D. (2015). Fluoxetine suppresses calcium signaling in human T lymphocytes through depletion of intracellular calcium stores. Cell Calcium, 58(3), 254–263. https://doi.org/10.1016/j.ceca.2015.06.003

Register to see more suggestions

Mendeley helps you to discover research relevant for your work.

Already have an account?

Save time finding and organizing research with Mendeley

Sign up for free