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dc.contributor.authorBUNTINX, Mieke-
dc.contributor.authorAMELOOT, Marcel-
dc.contributor.authorSTEELS, Paul-
dc.contributor.authorJANSSEN, Paul-
dc.contributor.authorMEDAER, Rob-
dc.contributor.authorGEUSENS, Piet-
dc.contributor.authorRAUS, Jef-
dc.contributor.authorSTINISSEN, Piet-
dc.identifier.citationArchives of Physiology and Biochemistry, 113, p. B5-B5-
dc.description.abstractAutoreactive T lymphocytes are considered to play a crucial role in orchestrating an immunopathological cascade that culminates in damage to the myelin sheath, oligodendrocytes and axons in the central nervous system (CNS) of multiple sclerosis (MS) patients. Autoreactive T cells may also initiate a chronic inflammation in the joints of rheumatoid arthritis (RA) patients. However, autoreactive T cells appear to be only a small component of this immune infiltrate. It has been suggested that the majority of T cells are nonspecifically recruited into the CNS of MS patients and into the inflamed joint of RA patients. The mechanisms underlying the peripheral activation of non-autoantigen specific T cells in MS and RA and their clinical relevance remain however largely unknown. Several lines of evidence indicate that interferon-gamma (IFN-g) may play an important role in the pathogenesis of MS and RA. Here, we have studied whether T cells from patients with autoimmune diseases are more susceptible to T cell activation in the presence of IFN-g. We studied the effects of IFN-g on Ca2+-release from intracellular stores and Ca2+-influx from the extracellular environment in peripheral blood T cells from MS and RA patients, patients with common viral infections (flu-like symptoms) and healthy donors. Fluorescence imaging microscopy was used to monitor the intracellular [Ca2+]i signal in individual T cells. Our results indicate that IFN-g mediates a sustained elevated [Ca2+]i in T cells of (active) MS and RA patients as compared to healthy controls and flu patients. Furthermore, no [Ca2+]i increase was observed in Ca2+-free medium, excluding an effect of IFN-g on Ca2+-release from intracellular stores. Although this IFN-g-activated Ca2+-influx seems to be insufficient to induce T cell proliferation in vitro, our data indicate that proliferation in response to suboptimal doses of phytohemagglutine can significantly be augmented in the presence of IFN-g. This study suggests that the Ca2+-influx stimulated by IFN-g can act as a complementary mechanism in the activation of non-autoantigen specific T cells in the blood of patients affected by autoimmune disorders as MS and RA.-
dc.titleInterferon-gamma-induced Ca2+-influx in T lymphocytes of Multiple Sclerosis and Rheumatoid Arthritis patients: A complementary mechanism for T cell activation?-
dc.typeJournal Contribution-
item.fullcitationBUNTINX, Mieke; AMELOOT, Marcel; STEELS, Paul; JANSSEN, Paul; MEDAER, Rob; GEUSENS, Piet; RAUS, Jef & STINISSEN, Piet (2001) Interferon-gamma-induced Ca2+-influx in T lymphocytes of Multiple Sclerosis and Rheumatoid Arthritis patients: A complementary mechanism for T cell activation?. In: Archives of Physiology and Biochemistry, 113, p. B5-B5.-
item.fulltextNo Fulltext-
item.accessRightsClosed Access-
item.contributorGEUSENS, Piet-
item.contributorSTINISSEN, Piet-
item.contributorJANSSEN, Paul-
item.contributorRAUS, Jef-
item.contributorSTEELS, Paul-
item.contributorAMELOOT, Marcel-
item.contributorMEDAER, Rob-
item.contributorBUNTINX, Mieke-
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