Please use this identifier to cite or link to this item:
Title: Interferon-gamma-induced Ca2+-influx in T lymphocytes of Multiple Sclerosis and Rheumatoid Arthritis patients: A complementary mechanism for T cell activation?
Authors: BUNTINX, Mieke 
AMELOOT, Marcel 
RAUS, Jef 
Issue Date: 2001
Source: JOURNAL OF NEUROIMMUNOLOGY, 118 (1), p. 94-94
Abstract: Autoreactive T-lymphocytes are considered to play a crucial role in orchestrating a chronic inflammation in the central nervous system CNS Ž . of multiple sclerosis MS patients and in the joints of rheumatoid Ž . arthritis RA patients. However, it has been suggested that the majority Ž . of T-cells in the immune infiltrate are nonspecifically recruited into the CNS and into the inflamed joint, respectively. Furthermore, several lines of evidence suggest an important role for interferon-g Ž . IFN-g in the pathogenesis of MS and RA. Here, we have studied whether peripheral blood T-cells from patients with autoimmune diseases are more susceptible to activation in the presence of IFN-g. The results indicate that IFN-g w mediates a sustained elevated Ca in T-cells of active MS and RA 2q x Ž . i patients as compared to healthy controls and patients with common viral w 2q x 2q infections. No Ca increase was observed in Ca -free medium, i excluding an effect of IFN-g on Ca 2q -release from intracellular stores. Although the IFN-g-activated Ca 2q 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-g. This study suggests that the IFN-g-induced Ca 2q influx can act as a complementary mechanism in the activation of blood T-lymphocytes from MS and RA patients.
Document URI:
ISSN: 0165-5728
e-ISSN: 1872-8421
DOI: 10.1016/S0165-5728(01)00353-8
Category: M
Type: Journal Contribution
Appears in Collections:Research publications

Show full item record

Page view(s)

checked on May 20, 2022

Google ScholarTM



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