In order to verify whether Epstein-Barr virus (EBV)-induced polyclonal B cell activation is the major cause of autoimmunity during infectious mononucleosis (IM), we have investigated, by immunoblotting, the fine specificity of anti-smooth muscle autoantibodies (autoAbs) in the sera of IM patients. Furthermore, we have isolated a number of in vivo infected EBV-positive cell lines from a patient with IM and compared the reactivity of the secreted immunoglobulins (Igs) with that of serum autoAbs. The reactivity of anti-smooth muscle autoAbs was found to be closely restricted to three proteins of approximate molecular weights 54, 52 and 48 kD. Furthermore, none of 48 EBV-positive B cell lines shared any reactivity with serum autoantibodies. Taken together, these results suggest that EBV-induced autoimmunity is not a consequence of a random activation of B cells, but a specific phenomenon, requiring mechanisms other than polyclonal B cell activation.

MECHANISMS OTHER THAN POLYCLONAL B-CELL ACTIVATION POSSIBLY INVOLVED IN EPSTEIN-BARR VIRUS-INDUCED AUTOIMMUNITY

GARZELLI, CARLO;BASOLO, FULVIO;
1989-01-01

Abstract

In order to verify whether Epstein-Barr virus (EBV)-induced polyclonal B cell activation is the major cause of autoimmunity during infectious mononucleosis (IM), we have investigated, by immunoblotting, the fine specificity of anti-smooth muscle autoantibodies (autoAbs) in the sera of IM patients. Furthermore, we have isolated a number of in vivo infected EBV-positive cell lines from a patient with IM and compared the reactivity of the secreted immunoglobulins (Igs) with that of serum autoAbs. The reactivity of anti-smooth muscle autoAbs was found to be closely restricted to three proteins of approximate molecular weights 54, 52 and 48 kD. Furthermore, none of 48 EBV-positive B cell lines shared any reactivity with serum autoantibodies. Taken together, these results suggest that EBV-induced autoimmunity is not a consequence of a random activation of B cells, but a specific phenomenon, requiring mechanisms other than polyclonal B cell activation.
1989
Garzelli, Carlo; Pacciardi, A; Basolo, Fulvio; Falcone, G.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11568/173196
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