Thyroid hormones as modulators of immune activities at the cellular level.

Increasing evidence suggest that thyroid hormones, namely thyroxine (T4) and 3,3’,5-triiodo-L-thyronine (T3), contribute to modulate the immune response. An array of monocyte, macrophage and leukocyte functions, such as chemotaxis, phagocytosis, Reactive Oxygen Species (ROS) generation, cytokine synthesis and release seem to be strictly dependent on hypo- or hyperthyroid status. It is well known that hyperthyroidism lowers the proinflammatory activities of monocytes and macrophages, whereas under hypothyroid condition activities such as phagocytosis and ROS generation appear to be enhanced. Similarly the expression of inflammatory molecules such as protein-1 α and interleukin-1β appear to increase in hypothyroidism. However, in Kupffer cells, proinflammatory activities such as respiratory burst as well as nitric oxide synthase activity and tumor necrosis factor alpha expression seem to be positively coupled to an increase of T3 levels. Both innate and adaptive components of the immune system undergo significant age-related changes and the effects of thyroid hormones on natural killer cell activity as well as humoral and cell-mediated immune responses provide a new insight into the mechanisms by which the endocrine system can affect the biological activity of these cells. Since the interactions between thyroid hormones and immune system as a whole are definitely complex, aim of this review is to outline the contribution of thyroid hormones to different aspects of innate and adaptive immune response such as chemotaxis, phagocytosis, respiratory burst, and cytokines synthesis in cells of the immune system: monocytes, macrophages, leukocytes, natural killer, and lymphocytes. Future research about the molecular signalling mechanism involved in this cross-talk between thyroid hormones and immune system can be useful to develop new strategy to improve overall quality of life.