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The function of Fas, FasL and Bcl- 2 in the pathogenesis of autoimmune thyroid disorders / 中国病理生理杂志
Chinese Journal of Pathophysiology ; (12)1986.
Article in Chinese | WPRIM | ID: wpr-522276
ABSTRACT

AIM:

To investigate the expression and function of apoptosis-related protein, Fas, FasL, and Bcl-2 in the pathogenesis of autoimmune thyroiditis.

METHODS:

Immunohistochemical staining was performed on 20 Hashimoto's thyroiditis (HT), 20 Graves' disease (GD), and 20 thyroid follicular adenoma (TFA, as control).

RESULTS:

All the cases expressed Fas, mainly on the cell surface and cytoplasm. FasL was found in all except 3 of the TFA. Bcl-2 in 15 of HT, 19 of GD, 17 of TFA. In TFA follicular cells expressed moderate Fas and minimal or absent FasL. In HT, follicles adjacent to infiltrating lymphocytes showed a increased levels of Fas and FasL, but infiltrating lymphocytes exhibited weaker staining of Fas and FasL than thyrocytes. In GD, thyrocytes and lymphocytes showed nearly similar Fas with HT, but rather weaker for FasL than HT. Bcl-2 was nearly similar in GD and TFA, but follicular cells in vicinity of lymphocytes and lymphocytes located in germinal centers of HT tissues exhibited significantly weaker.

CONCLUSION:

The expression of Fas, FasL and Bcl-2 in Hashimoto's thyroiditis and Graves' disease was nearly similar. Strong FasL expression and weak Bcl-2 expression on the follicles in HT may induce apoptosis. These results provide further proof that the functions of Fas and its ligand and Bcl-2 may play an important part in the pathogenesis of autoimmune thyroid diseases. The lymphocytes do not seem to be directly engaged in the process with their own FasL, but they may provide some cytokines that, in turn, up-regulates Fas and/or FasL leading to apoptosis.

Full text: Available Index: WPRIM (Western Pacific) Type of study: Etiology study Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 1986 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Type of study: Etiology study Language: Chinese Journal: Chinese Journal of Pathophysiology Year: 1986 Type: Article