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. 1989 Jun;76(3):412–416.

Mechanisms other than polyclonal B cell activation possibly involved in Epstein-Barr virus-induced autoimmunity.

C Garzelli 1, A Pacciardi 1, F Basolo 1, G Falcone 1
PMCID: PMC1541886  PMID: 2546702

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.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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