Androgen‐dependent expression of FcγRIIB2 by thyrocytes from patients with autoimmune Graves' disease: a possible molecular clue for sex dependence of autoimmune disease

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Abstract
Thyrocyte expression of HLA class I and class II antigens and related accessory molecules would convert these epithelial cells into functional antigen-presenting cells. Here we show that whereas normal thyrocytes express FcRn, Graves’ disease thyrocytes also express FcγRIIB2. We further find that expression of FcγRIIB2, but not FcRn, is repressed by dihydrotestosterone. By mediating the uptake and transport of autoantibodies, we suggest that these IgG Fc receptors contribute in various ways to the onset and/or progression of autoimmune thyroid diseases. The androgen-mediated decrease of FcγRIIB2 expression in Graves’ disease thyrocytes also provides a rationale for the predominant susceptibility of women to develop an autoimmune thyroid disease. Our findings open up a new prospect to autoimmunity, linking the role of the target organ to the sex dependence in autoimmune disease.—Estienne, V., Duthoit, C., Reichert, M., Praetor, A., Carayon, P., Hunziker, W., Ruf, J. Androgen-dependent expression of FcγRIIB2 by thyrocytes from patients with autoimmune Graves’ disease: a possible molecular clue for sex dependence of autoimmune disease.
Funding Information
  • Federation of European Biochemical Societies