It is now widely accepted that thyroid hormones, l-thyroxine (T(4)) and 
3,3',5-triiodo-l-thyronine (T(3)), act as modulators of the immune response. 
Immune functions such as chemotaxis, phagocytosis, generation of reactive oxygen 
species, and cytokine synthesis and release, are altered in hypo- and 
hyper-thyroid conditions, even though for many immune cells no clear correlation 
has been found between altered levels of T(3) or T(4) and effects on the immune 
responses. Integrins are extracellular matrix proteins that are important 
modulators of many cellular responses, and the integrin αvβ3 has been identified 
as a cell surface receptor for thyroid hormones. Rapid signaling via this plasma 
membrane binding site appears to be responsible for many nongenomic effects of 
thyroid hormones, independent of the classic nuclear receptors. Through the 
integrin αvβ3 receptor the hormone can activate both the ERK1/2 and 
phosphatidylinositol 3-kinase pathways, with downstream effects including 
intracellular protein trafficking, angiogenesis and tumor cell proliferation. It 
has recently become clear that an important downstream target of the thyroid 
hormone nongenomic pathway may be the mammalian target of rapamycin, mTOR. New 
results demonstrate the capability of T(3) or T(4) to induce in the short time 
range important responses related to the immune function, such as reactive 
oxygen species production and cell migration in THP-1 monocytes. Thus thyroid 
hormones seem to be able to modulate the immune system by a combination of rapid 
nongenomic responses interacting with the classical nuclear response.