IMMUNOGLOBULIN PRODUCTION INDUCED BY CD57(-DERIVED HELPER T-CELLS IN-VITRO REQUIRES ADDITION OF EXOGENOUS IL-2() GC)

Citation
E. Andersson et al., IMMUNOGLOBULIN PRODUCTION INDUCED BY CD57(-DERIVED HELPER T-CELLS IN-VITRO REQUIRES ADDITION OF EXOGENOUS IL-2() GC), Cellular immunology, 169(2), 1996, pp. 166-173
Citations number
31
Categorie Soggetti
Cell Biology",Immunology
Journal title
ISSN journal
00088749
Volume
169
Issue
2
Year of publication
1996
Pages
166 - 173
Database
ISI
SICI code
0008-8749(1996)169:2<166:IPIBCH>2.0.ZU;2-P
Abstract
Germinal centers (GC) are well-defined areas in lymphoid organs were B cells proliferate and differentiate in response to T-cell-dependent a ntigens. The GC comprises B cells, follicular dendritic cells, tangibl e body macrophages, and a low number of CD4(+) T cells. A large portio n of these T cells expresses CD57. We have examined the ability of the CD4(+)CD57(+) GC T cells to become activated and to take part in B ce ll activation processes. These T cells coexpress CD45RO, CD69, CD28, a nd upon mitogenic stimulation CD25. The cell population was found neit her to containe nor to be able to produce any specific mRNA for IL-2, IL-4, and IFN-gamma upon activation. Levels of mRNA encoding CD40 liga nd was also undetectable under similar conditions. Furthermore, in con trast to ordinary CD4(+) T cells, this population expressing CD57 was unable to induce B cells to Ig production in the presence of pokeweed mitogen or SEA unless IL-2 was added to the cultures, However, despite their apparent lack of function CD4(+)CD57(+) GC T cells were found t o rescue GC B cells from cell death in vitro to the same extent as CD4 (+)CD57(-) T-h cells. The phenotypical and functional differences foun d between these T cells and regular T-h-cells suggest that they either represent a T cell subset with distinct properties within the GC yet to be determined or that they represent T cells, late in the immune re sponse, having lost most of their original functions and capabilities. (C) 1996 Academic Press, Inc.