Polyspecific immunoglobulins (IVIg) suppress proliferation of human (auto)antigen-specific T cells without inducing apoptosis.
Polyspecific immunoglobulins (IVIg) have been shown to reduce disease activity in multiple sclerosis (MS). To investigate the mechanisms of action of IVIg, we studied the impact of IVIg on growth and death (apoptosis) of human (auto)antigen-specific T cells. We observed a substantial suppression of proliferation of specifically activated T cells, in absence of caspase activation or DNA fragmentation. Further, neither susceptibility of T cells to undergo CD95-mediated apoptosis nor expression of apoptosis-blocking bcl-2 was modulated by IVIg. We conclude that IVIg may inhibit the reactivity of antigen-specific T cells in MS through suppression of proliferation rather than modulation of apoptosis.
Department of Neurology, Division of Neuroimmunology, University Hospital Charité, NWFZ 2680, Schumannstrasse 20/21, 10117 Berlin, Germany.
O
O
Aktas
S
S
Waiczies
U
U
Grieger
U
U
Wendling
R
R
Zschenderlein
F
F
Zipp
D017209:Apoptosis / Q000276:immunology*; D001324:Autoantigens / Q000276:immunology*; D002455:Cell Division / Q000276:immunology; D002460:Cell Line; D000939:Epitopes; D006801:Humans; D016756:Immunoglobulins, Intravenous / Q000276:immunology* / Q000494:pharmacology; D066298:In Vitro Techniques; D009103:Multiple Sclerosis / Q000276:immunology; D013601:T-Lymphocytes / Q000166:cytology* / Q000276:immunology*; D019014:fas Receptor / Q000276:immunology
D001324:Autoantigens; D000939:Epitopes; D016756:Immunoglobulins, Intravenous; D019014:fas Receptor