The role of IgG4 (+) plasma cells in the association of Hashimoto's thyroiditis with papillary carcinoma

Apmis ◽  
2014 ◽  
Vol 122 (12) ◽  
pp. 1259-1265 ◽  
Author(s):  
Funda Taşli ◽  
Güliz Özkök ◽  
Asuman Argon ◽  
Didem Ersöz ◽  
Ayşe Yağci ◽  
...  
2018 ◽  
Author(s):  
B Ramesh ◽  
B Rajesh ◽  
Reddy B Rajkiran ◽  
G Gayathri ◽  
Reddy M Venkateshwara ◽  
...  

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Aleksandra Pyzik ◽  
Ewelina Grywalska ◽  
Beata Matyjaszek-Matuszek ◽  
Jacek Roliński

This review of literature attempts to identify the factors that are involved in the pathogenesis of Hashimoto thyroiditis, an immune defect in an individual with genetic susceptibility accompanied with environmental factors. The frequency of Hashimoto’s disease is a growing trend and among Caucasians it is estimated at approximately 5%. The dysfunction of the gland may be clinically evident (0.1–2% of the population) or subclinical (10–15%). The pathology is diagnosed five to ten times more often in women than men and its incidence increases with the age (the peak of the number of cases is between 45 and 65); however, it can also be diagnosed in children. The pathogenesis of Hashimoto’s thyroiditis is still not fully comprehended. In the etiology of Hashimoto thyroiditis excessively stimulated T CD4+ cells are known to play the most important role. Recent research has demonstrated an increasing role of newly discovered cells such as Th17 (CD4+IL-17+) or T regulatory cells (CD4+CD25+highFoxP3+) in the induction of autoimmune disorders. The process of programmed cell death also plays an equally important role in the pathogenesis and the development of hypothyroidism.


Grossly, thyroid enlargement in Hashimoto's thyroiditis (HT) is generally symmetrical, often with a characteristic conspicuous pyramidal lobe. The tissue involved by HT is pinkish-tan to frankly yellowish in color and tends to have a rubbery firmness. There is no necrosis or calcification. The capsule is intact and non-adherent to peri-thyroid structures. Microscopically, there is a diffuse process consisting of a combination of epithelial cell destruction, lymphoid cellular infiltration, and fibrosis. Lymphocytes are predominantly T-cells and plasma cells. Most infiltrating T-cells have α/β T-cell receptors. Gamma/delta T-cells are rare. Hashimoto's thyroiditis has been graded based on lymphocytic infiltration seen on cytology, into Grades 0-III, where Grade 0 means no lymphoid cells and Grade III severe lymphoid cell infiltration. Deposits of dense material representing IgG are found along the basement membrane on electron microscopy. This chapter explores the pathology of Hashimoto's disease.


2018 ◽  
Vol 44 (6) ◽  
pp. 1164-1169 ◽  
Author(s):  
Zi-mei Lin ◽  
Yao Wang ◽  
Chun-mei Liu ◽  
Cao-xin Yan ◽  
Pin-tong Huang

CHEST Journal ◽  
2014 ◽  
Vol 145 (3) ◽  
pp. 292A
Author(s):  
Francina Bolanos ◽  
Emmanuel Peña Gomezportugal ◽  
Enrique Guzman del alba ◽  
Patricio Santillán Doherty ◽  
Fortunato Juarez

2001 ◽  
pp. 561-568 ◽  
Author(s):  
M Andrikoula ◽  
A Tsatsoulis

Recent evidence has emphasized the importance of apoptosis in the maintenance of tissue homeostasis and the pathogenesis of malignant and immune diseases. Autoimmune thyroid diseases such as Hashimoto's thyroiditis and Graves' disease, as well as other autoimmune endocrine diseases, have been associated with dysregulation of apoptotic signaling pathways. In particular, dysfunction of the Fas apoptotic pathway or production of soluble factors including soluble Fas and soluble Fas ligand may be involved in the pathogenesis of these disorders. On the other hand, malignant thyroid cells may avoid Fas-mediated suicide possibly by expression of inhibitors of apoptosis and evade the immune system by inducing apoptosis on infiltrating lymphocytes. The delicate balance between cell proliferation and cell death through the Fas pathway may also play an important role in the control of thyroid cell mass and goitrogenesis. This review analyzes the current evidence on the role of Fas-mediated apoptosis in the pathogenesis of thyroid diseases including Hashimoto's thyroiditis, Graves' disease, thyroid cancer and goiter. However, the exact mechanisms involved in the regulation of apoptosis in thyroid disease remain unclear. Further investigation is needed.


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