Mechanisms other than polyclonal B cell activation possibly involved in Epstein-Barr virus-induced autoimmunity.
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.
Garzelli
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C
Department of Biomedicine, University of Pisa, Italy.
Pacciardi
A
A
Basolo
F
F
Falcone
G
G
D000918:Antibody Specificity; D001323:Autoantibodies / Q000032:analysis; D001327:Autoimmune Diseases / Q000209:etiology / Q000276:immunology*; D001402:B-Lymphocytes / Q000276:immunology*; D002461:Cell Line, Transformed; D005455:Fluorescent Antibody Technique; D004854:Herpesvirus 4, Human / Q000276:immunology*; D006801:Humans; D015151:Immunoblotting; D007244:Infectious Mononucleosis / Q000276:immunology*; D008213:Lymphocyte Activation; D009130:Muscle, Smooth / Q000276:immunology
D001323:Autoantibodies