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|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|
|Issue Date: ||2001|
|Citation: ||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 .
patients as compared to healthy controls and patients with common viral
infections. No Ca increase was observed in Ca -free medium,
excluding an effect of IFN-g on Ca
-release from intracellular stores.
Although the IFN-g-activated Ca
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
influx can act as a
complementary mechanism in the activation of blood T-lymphocytes
from MS and RA patients.|
|Type: ||Journal Contribution|
|Appears in Collections: ||Research publications|
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