1
Views
2
CrossRef citations to date
0
Altmetric
Research Article

Augmentation of Cytotoxicity by Splenic Cells of Pregnant or Human Chorionic Gonadotropin-Treated Normal Mice

, , &
Pages 309-324 | Published online: 28 Sep 2008
 

Abstract

The natural killer (NK) activity, of an allogeneic tumor system, was found to be enhanced by the total splenic population of either pregnant or normal female BALB/c mice treated with human chorionic gonadotropin (HCG). The splenic population of the early pregnant (9-10 days) mice resulted in a statistically significant increase in NK activity over nonpregnant controls at all effector/ target ratios tested. The mid (12-13 days) and the late (15-16 days) pregnant groups also significantly enhanced NK activity above control values at effector/target ratios of 100:1, 50:1 and 25:1. The i.v. administration of carrageenan into pregnant mice abolished the increased NK activity suggesting a putative role for the macrophage in this system. HCG administered to normal female BALB/c mice resulted in enhanced NK activity similar to that seen for the pregnant mice. This augmented NK activity does not appear to be effected by either the number or the timing of HCG administration. The augmentation of NK activity of HCG treated mice was also detected in a syngeneic system utilizing 51Cr labeled M109 tumor target cells and BALB/c effector cells.

Reprints and Corporate Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

To request a reprint or corporate permissions for this article, please click on the relevant link below:

Academic Permissions

Please note: Selecting permissions does not provide access to the full text of the article, please see our help page How do I view content?

Obtain permissions instantly via Rightslink by clicking on the button below:

If you are unable to obtain permissions via Rightslink, please complete and submit this Permissions form. For more information, please visit our Permissions help page.