Document Server@UHasselt >
Research publications >
Please use this identifier to cite or link to this item:
|Title: ||Interferon-gamma-induced calcium influx in T lymphocytes of multiple sclerosis and rheumatoid arthritis patients: a complementary mechanism for T cell activation?|
|Authors: ||BUNTINX, Mieke|
|Keywords: ||Clinical trials|
|Issue Date: ||2002|
|Citation: ||Journal of Neuroimmunology, 124(1-2). p. 70-82|
|Abstract: ||Autoreactive T lymphocytes are considered to play a crucial role in orchestrating a chronic inflammation in the central nervous system (CNS) of multiple sclerosis (MS) patients and in the joints of rheumatoid arthritis (RA) patients. However, it has been suggested that the majority of T cells in the immune infiltrate are nonspecifically recruited into the CNS and into the inflamed joint. In addition, several lines of evidence suggest an important role for interferon-γ (IFN-γ) in the pathogenesis of MS and RA. We have studied whether peripheral blood T cells from patients with autoimmune diseases are more susceptible to activation in the presence of IFN-γ. The results indicate that IFN-γ mediates a sustained elevated [Ca2+]i in T cells of (active) MS and RA patients as compared to healthy controls and patients with common viral infections. No [Ca2+]i increase was observed in Ca2+-free medium, excluding an effect of IFN-γ on Ca2+-release from intracellular stores. Although the IFN-γ-activated Ca2+-influx is insufficient to induce T cell proliferation in vitro, our data indicate a significantly augmented proliferation in response to suboptimal doses of PHA in the presence of IFN-γ. This study suggests that the IFN-γ-induced Ca2+-influx can act as a complementary mechanism in the activation of blood T lymphocytes from MS and RA patients.|
|ISI #: ||000174688600010|
|Type: ||Journal Contribution|
|Validation: ||ecoom, 2003|
|Appears in Collections: ||Research publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.