The essential trace mineral selenium is of fundamental importance to human 
health. It is incorporated in the proteome in the forms of the genetically 
encoded amino acids selenocysteine and selenomethionine, which are the 
characteristic components of selenoproteins (SeP) such as glutathione 
peroxidases (GPx), thioredoxin reductases and iodothyronine deiodinase families. 
Thyroid is especially sensitive to selenium deficiency, because SeP can modify 
thyreocytes function by acting as antioxidants and modifying redox status and 
thyroid hormone metabolism. SeP are also involved in apoptosis, cell growth and 
modification of the action of cell signalling systems and transcription factors. 
Some intestinal GPx modulate apoptosis by removing the cells affected by 
oxidative damage preserving tissue integrity. The malfunctioning of the GPx 
antioxidant system in intestinal mucosa can trigger a continuous cycle of 
reactive oxygen species and inflammation. Selenium deficiency is a risk factor, 
due to the malabsorption, in celiac disease (CD) because the inflammatory damage 
affects the small intestine; this deficiency can modulate SeP genes expression, 
with consequent reiteration of inflammation and increase of mucosal damage. In 
active CD, overexpression of interleukin-15 (IL-15) may increase activation of 
effector mechanisms of epithelial damage by stimulating T helper 1 cytokine 
proliferation and production and intraepithelial lymphocytes cytotoxicity by 
protecting these lymphocytes from apoptosis. Blocking IL-15 has the potential to 
provide new therapeutic tools to prevent both tissue damage and complication of 
CD such as autoimmune thyroid diseases (AITD) where IL-15 expression is also 
increases. In view of the role played by SeP in apoptosis inhibition, the 
presence of environmental factors such as selenium deficiency can be considered 
an important direct factor of thyroidal damage in development of AITD.