Please use this identifier to cite or link to this item:
Title: Biphasic activity of cd137 ligand-stimulated monocytes on T cell apoptosis and proliferation
Authors: Shaqireen Kwajah, M.M.
Mustafa, N.
Holme, A.L. 
Pervaiz, S.
Schwarz, H.
Keywords: Cell death
Reactive oxygen species
Issue Date: May-2011
Source: Shaqireen Kwajah, M.M., Mustafa, N., Holme, A.L., Pervaiz, S., Schwarz, H. (2011-05). Biphasic activity of cd137 ligand-stimulated monocytes on T cell apoptosis and proliferation. Journal of Leukocyte Biology 89 (5) : 707-720. ScholarBank@NUS Repository.
Abstract: CD137L (4-1BBL) is a member of the TNFSF and is expressed on APCs as a transmembrane protein. Reverse signaling by CD137L in monocytes causes cell activation and differentiation to mature inflammatory DCs that can stimulate T cell proliferation. However, CD137L agonists have also been reported to induce apoptosis in PBMCs. This study aimed at clarifying these seemingly opposing activities. We find that the dying cells within PBMCs are T cells and that this T cell death is dependent on monocytes and correlates with the monocyte:T cell ratio. This CD137L-induced, monocytemediated T cell apoptosis is reminiscent of MDCD, and both are cell contact-dependent. T cell death is not mediated by CD95 or DR4 or -5 but by ROS produced by the T cells. T cell apoptosis is restricted to the first 24 h of stimulation, and at later time-points, the monocytes differentiate to inflammatory DCs under the influence of CD137L signaling and acquire the capacity to stimulate T cell proliferation from Day 4 onward. This biphasic activity may contribute to infection-induced T cell attrition, where in the early phase (
Source Title: Journal of Leukocyte Biology
ISSN: 07415400
DOI: 10.1189/jlb.1010569
Appears in Collections:Staff Publications

Show full item record
Files in This Item:
There are no files associated with this item.


checked on Feb 26, 2018


checked on Feb 26, 2018

Page view(s)

checked on Feb 25, 2018

Google ScholarTM



Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.