Analysis of the Expression of Fas,FasL and Bcl-2 in the Pathogenesis of Autoimmune Thyroid Disorders

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To investigate the expression of apoptosis-related protein(Fas,FasL,and Bcl-2)in the pathogenesis ofautoimmune thyroid disorders (ATDs),immunohistochemical staining was performed on 20 Hashimoto’sthyroiditis(HT),20 Graves’disease(GD),and 20 thyroid follicular adenoma(TFA,as control).All the casesexpressed Fas,mainly on the cell surface and cytoplasm.FasL was found in 17 cases of the TFA.Bcl-2 wasdetected in 15 cases of HT,19 of GD and 17 of TFA.In TFA,a moderate Fas expression and a minimal or noFasL expression was detected on follicular cells.In HT,the follicles adjacent to infiltrating lymphocytes showedincreased levels of Fas and FasL expression.A weaker staining of Fas and FasL was exhibited on infiltratinglymphocytes than on thyrocytes.In a comparison of GD with HT,thyrocytes and lymphocytes showed similarFas staining,but for FasL the staining was rather weaker in HT.The expression of Bcl-2 was nearly identical inGD and TFA,but much weaker on the follicular cells in vicinity of lymphocytes and on the lymphocytes locatedin germinal centers of HT tissues.The expression of Fas,FasL,Bcl-2 in Hashimoto’s thyroiditis and Graves’disease were almost same.FasL strong expression and Bcl-2 weak expression on the follicles in HT may induceapoptosis.These results provided evidence for expression of Fas,FasL and Bcl-2 in the pathogenesis ofautoimmune thyroid disease.The lymphocytes seem not to be directly engaged in the process via their ownFasL,but they may provide some cytokines that,in turn,upregulate Fas and/or FasL expression to induceapoptosis.Cellular & Molecular Immunology.2004;1(3):224-228. To investigate the expression of apoptosis-related protein (Fas, FasL, and Bcl-2) in the pathogenesis of autoimmune thyroid disorders (ATDs), immunohistochemical staining was performed on 20 Hashimoto’sthyroiditis (HT), 20 Graves’disease and 20 thyroid follicular adenoma (TFA, as control). All the casesexpressed Fas, mainly on the cell surface and cytoplasm. FasL was found in 17 cases of the TFA.Bcl-2 wasdetected in 15 cases of HT, 19 of GD and 17 of TFA. TFA, a moderate Fas expression and a minimal or no FasL expression was detected on follicular cells. In HT, the follicles adjacent to infiltrating lymphocytes showedincreased levels of Fas and FasL expression. A weaker staining of Fas and FasL was exhibited on infiltrating lymphocytes than on thyrocytes. a a comparison of GD with HT, thyrocytes and lymphocytes showed similarFas staining, but for FasL the staining was rather weaker in HT. expression of Bcl-2 was nearly identical inGD and TFA, but much weaker on the follicular cells in vicinity of ly mphocytes and on the lymphocytes located in germinal centers of HT tissues. The expression of Fas, FasL, Bcl-2 in Hashimoto’s thyroiditis and Graves’ disease were almost same. FasL strong expression and Bcl-2 weak expression on the follicles in HT may induce apoptosis. These results provide evidence for expression of Fas, FasL and Bcl-2 in the pathogenesis of autoimmune thyroid disease. The lymphocytes seem not to be directly engaged in the process via their own FasL, but they may provide some cytokines that, in turn, upregulate Fas and / or FasL expression to induceapoptosis. Cellular & Molecular Immunology. 2004; 1 (3): 224-228.
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