FAS AND FASL ARE INVOLVED IN THE PATHOGENESIS OF
AUTOIMMUNE THYROID DISEASE
Zhang HW, Lin HH
Pediatrics, Tongji Hospital, Wuhan, China
Objective:
Apoptosis via the Fas pathway is supposed to be a potential mechanism for
the autoimmune thyroid disease. Rescent studies reported contradictory
results regarding the expression of Fas/FasL by thyrocyte in two
pathologically different autoimmune thyroid disease.Therefore we
constructed a delicate design to study the expression of Fas/FasL by
thyrocyte.
Method: Archival
formalin-fixed and paraffin-embeded thyroid specimens from 20 patients with
Hashimoto’s thyroiditis or Graves disease, were retrieved retrospectively from the files of the pathology
department. We used two different techniques (PAP and immunoflur escent
method ) and two different antibodies (NOK-1 and Q-20) to determine the
expression of FasL. Graves’ thyroid
tissue and non-toxic thyroid nodule tissue were obtained from seven
patients at the time of subtotal thyroidectomy. After seven days of primary
thyrocyte culture, IFN-γ, TNF-αor IL-1β was added to study their influences on the
expression of Fas.
Result:
FasL was detected by the two antibodies in Graves’ disease and non –toxic
diffuse thyroid nodule. Q-20 can detect FasL in Hashimoto’s thyroiditis,
but NOK-1 can not. Fas was increased by TNF-αor IL-1β,but not by IFN-γ.Fas was decreased by TSH.
Conclusion: Thyroid is a immune-privileged organ. Loss
of functional FasL in thyrocytes
may lead to accumulation of lymphocytes in Hashimoto’s thyroiditis. Downregulation
of Fas by TSH may be involved in the hyperplasia of thyrocytes in Graves’
disease. TNF-αand IL-1βinduced Fas upregulation may be contributed
suicide or paracide of thyrocytes in Hashimoto’s thyroiditis.