Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Search research articles

Related Experiment Videos

Serotonin modulated Ca++ dependent K+ channels in alloimmune effector cell lytic function.

A Liepins¹, A LeFever, R L Truitt

¹Memorial University, Faculty of Medicine, St. John's, Newfoundland, Canada.

Immunopharmacology and Immunotoxicology

|January 1, 1989

Summary

This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by

Same author

The determination of endotoxin in the finished cellular product.

Cytotherapy·2010

Same author

Rapamycin enriches for CD4(+) CD25(+) CD27(+) Foxp3(+) regulatory T cells in ex vivo-expanded CD25-enriched products from healthy donors and patients with multiple sclerosis.

Cytotherapy·2007

Same author

Role of Bcl-2 family proteins and caspase-3 in sanguinarine-induced bimodal cell death.

Cell biology and toxicology·2002

Same author

Donor natural killer (NK1.1+) cells do not play a role in the suppression of GVHD or in the mediation of GVL reactions after DLI.

Biology of blood and marrow transplantation : journal of the American Society for Blood and Marrow Transplantation·2002

Same author

Sanguinarine induces bimodal cell death in K562 but not in high Bcl-2-expressing JM1 cells.

Pathology, research and practice·2002

Same author

Bax, Bcl-2, and NF-kappaB expression in sanguinarine induced bimodal cell death.

Experimental and molecular pathology·2001

Same journal

Correction.

Immunopharmacology and immunotoxicology·2026

Same journal

Immuno-regulatory effects of hydroxychloroquine in experimental autoimmune thyroiditis.

Immunopharmacology and immunotoxicology·2026

Same journal

From the lab to the feed: science communication through an immunological lens in the social media era.

Immunopharmacology and immunotoxicology·2026

Same journal

Systemic administration of interleukin-10 is associated with dose-dependent toxicities in Wistar albino rats.

Immunopharmacology and immunotoxicology·2026

Same journal

Nano-enabled strategies for enhancing cancer immunotherapy: challenges, progress and perspective.

Immunopharmacology and immunotoxicology·2026

Same journal

Statement of Retraction: Amygdalin Induces Apoptosis in Human Cervical Cancer Cell Line HeLa Cells.

Immunopharmacology and immunotoxicology·2026

See all related articles

Potassium channel blockers, including serotonin (5-HT) and quinidine, inhibit immune cell killing of tumor cells. These findings suggest neuroendocrine products modulate lymphocyte function via 5-HT sensitive, calcium-dependent potassium channels.

Area of Science:

Immunology
Neuroendocrinology
Cellular Physiology

Background:

Potassium channel activity is crucial for the cytotoxic function of immune effector cells like T lymphocytes and NK cells.
Tumor cell injury is also linked to ion channel activity, suggesting a broader role in cell-mediated cytotoxicity.

Purpose of the Study:

To investigate the impact of various potassium (K+) channel blockers on the cytolytic activity of in vivo derived alloimmune lymphocytes against P815 tumor cells.
To determine if serotonin (5-HT) sensitive, calcium-dependent K+ channels are involved in lymphocyte-mediated lysis.

Main Methods:

Utilized K+ channel blockers: 4-aminopyridine (4-AP), serotonin (5-HT), quipazine (5-HT agonist), and quinidine (Ca++ dependent K+ channel blocker).
Assessed tumor cell lysis via 51Cr release assay.

Related Experiment Videos

Compared inhibition effects of preincubating effector cells versus target cells with blockers.

Main Results:

All tested K+ channel blockers (4-AP, 5-HT, quipazine, quinidine) inhibited P815 tumor cell lysis in a dose-dependent manner.
Preincubation of effector lymphocytes with blockers yielded greater inhibition than preincubation of target cells.
Quipazine and quinidine demonstrated similar dose-dependent inhibition, suggesting involvement of 5-HT sensitive, Ca++ dependent K+ channels.

Conclusions:

5-HT sensitive, Ca++ dependent K+ channels are likely involved in mediating the lytic function of immune effector lymphocytes.
Neuroendocrine products, such as serotonin, may play a role in modulating the functional activity of lymphocytes derived from in vivo studies.