Abstract
Over the past few years, growing evidence suggests direct crosstalk between thyroid hormones (THs) and the immune system. Components of the immune system were proposed to interfere with the central regulation of systemic TH levels. Conversely, THs regulate innate and adaptive immune responses as immune cells are direct target cells of THs. Accordingly, they express different components of local TH action, such as TH transporters or receptors, but our picture of the interplay between THs and the immune system is still incomplete. This review provides a critical overview of current knowledge regarding the interaction of THs and the immune system with the main focus on local TH action within major innate and adaptive immune cell subsets. Thereby, this review aims to highlight open issues which might help to infer the clinical relevance of THs in host defence in the context of different types of diseases such as infection, ischemic organ injury or cancer.
Highlights
Thyroid hormones (THs) are critical regulators of various physiological processes within the human body, which become evident in case of imbalance
thyroid hormones (THs) were described to enhance the antibacterial immune response of monocyte-derived macrophages indicated by enhanced phagocytic activity as well as elevated expression of inducible nitric oxide synthase in these cells (58)
Many data are based on mRNA analysis whereas the knowledge on the “functional” expression of proteins involved in local TH action within immune cells is fragmentary, in part due to lack of specific antibodies, e.g. for THRa and THRb (Tab. 1)
Summary
Thyroid hormones (THs) are critical regulators of various physiological processes within the human body, which become evident in case of imbalance. THs may drive pro-inflammatory macrophage responses as they triggered phagocytic activity and nitric oxide (NO) production in murine and human macrophage cell lines (58). THs were described to enhance the antibacterial immune response of monocyte-derived macrophages indicated by enhanced phagocytic activity as well as elevated expression of inducible nitric oxide synthase (iNOS) in these cells (58).
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