Thyrotropin receptor antibody (TRAb) is a causative antibody of Graves‘ disease. Epstein-Barr virus (EBV) persists in human B cells, and occasionally reactivates. We have reported that both Graves‘ disease patients and healthy controls have EBV-infected B cells that have TRAb as their surface globulin (TRAb(+) EBV(+) cells). The peripheral blood mononuclear cells containing TRAb(+) EBV(+) cells produced TRAbs along with EBV reactivation. We proposed the EBV reactivation-induced Ig production as alternative system of Ig production.
The antibodies produced by EBV reactivation-induced system are IgM dominant, and skewed to be autoreactive. However, the class of thyroid stimulating TRAb is known to be IgG. We studied about the role of the IgM antibody.
We purified TRAb-IgM from culture medium of TRAb(+) EBV(+) cells. Then, we cultured porcine thyroid cells with the TRAb-IgM and complements, and then, measured cAMP and LDH levels to estimate thyroid stimulating effect and cell injury, respectively. We observed the increase of the levels of LDH, but could not detect cAMP.
We considered that TRAb-IgM did not have thyroid stimulating effect, but it could injure the thyroid cells and release thyroid antigens including TSH receptor antigen. The relevance of EBV reactivation to Graves‘ disease may have a possibility for the new therapy.