| Research Abstract |
CD5^+B cells and CD5^-B cells are present in a B cell subpopulation. We previously found that CD5^+B cells are increased in autoimmune thyroid disease as well as in other autoimmune diseases. The number of CD5^+B cells is increased more in the hyperthyroid state than in the euthyroid state in Graves' disease, and is correlated with the serum levels of thyroid hormones or thyroid autoantibodies. Therefore, we examined which subset of B cells produces thyroid autoantibodies, and whether thyroid hormones may increase CD5^+B cells.
We separated CD5^+B cells and CD5^-B cells from peripheral blood mononuclear cells from patients with autoimmune thyroid disease by using a cell sorter (FACStar). Each subset of B cells was cultured for 7 days with feeder cells of irradiated autologous lymphocytes in stimulation with B and T cell mitogens. Then, we clarified that CD5-B cells produce IgG-class of thyroid-peroxidase antibodies and of thyroglobulin antibodies by using ELISPOT assay. However, we did not identify a B cell subset producing TSH-receptor antibodies. Interestingly, IgM-class of thyroid autoantibodies was produced by both CD5^+B and CD5^-B cells.
On the other hand, we administrated thyroxine or PTU to C57BL/6J mice for 1-6 months to make hyper- or hypothyroid mice. Splenic lymphocyte subsets were examined by two-clour flow cytomotry. NK cells and T cells were increased in hyperthyroid mice, and CD5^-B cells were increased in hypothyroid mice. CD5^+B cells were did not change with the serum levels of thyroid hormone. Furthermore, CD5^+B cells decreased in patients with destructive thyrotoxicosis due to the aggravation of Hashimoto's disease, even though the serum levels of thyroid hormones increased.
These data suggest that CD5^+B cells may affect the production of thyroid-antibodies by CD5^-B cells, and that the increase of CD5^+B cells might be fundamental in the pathogenosis of Graves' disease.
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