Table 3.

Experimental therapeutic applications that target TGF-β physiology (synthesis, activation, action) in autoimmune thyroid diseases.

	Effect on Synthesis	Effect on Activation	Effect on Action	Experimental Therapeutic Application
Exogenously administrated hr-TGF-β	None	None	None	Cultures of follicular thyroid/lymphocyte cells from Graves’ disease in humans
Low-level laser therapy	Increase	None	None	Hashimoto’s thyroiditis in humans
Small peptides	None	Inhibit TGF-β disengagement from LAP	None	Cancer animal models
Monoclonal anti-TGF-β	None	None	Neutralize excess extracellular TGF-β	Hashimoto’s thyroiditis in animal models [61]
Triiodothyronine nuclear receptor ligands	None	None	Limit Smad phosphorylation	Thyroid fibrosis in animal models
Estrogen receptor β antagonists	None	None	Inhibit TGF-β-mediated Th17-type response	Experimental autoimmune thyroiditis in animal models
Estrogen receptor α agonists	None	None	Suppress TGF-β activity	Experimental autoimmune thyroiditis in animal models
COX-2 inhibitors	None	None	Block TGF-β-induced HA synthesis. Decrease TGF-β-induced ocular muscle fibroblasts proliferation	Cultures of extraocular muscle fibroblasts from TAO in humans
PPAR-γ agonists	Inhibit TNF- mediated TGF-β synthesis	None	Inhibit TGF-β-induced fibroblast differentiation to myofibroblasts.Decrease HAS and HA synthesis	Cultures of extraocular muscle fibroblasts from TAO in humans