Dean Sittig
For more than 70 years, glucocorticoids have been used to treat autoimmune and inflammatory diseases because of their potent anti-inflammatory and immune-suppressive properties. The severity of their side effects, which include osteoporosis, muscle wasting, hyperglycaemia, and hypertension, as well as the occurrence of resistance to glucocorticoid therapy, limit their use. An overview of our current understanding of the mechanisms underlying glucocorticoid treatments therapeutic and side effects, as well as the decreased sensitivity observed in resistant patients, is provided in this Special Issue. In addition, research that aims to either prevent or treat glucocorticoid resistance or to develop novel glucocorticoid therapies with fewer side effects is highlighted. The calming impacts of glucocorticoids are interceded by an intracellular receptor, the glucocorticoid receptor (GR). A wealth of information regarding which cells are the primary targets of the therapeutic effects of glucocorticoids has been provided by research conducted over the course of the past two decades using cell type-specific GR knockout mice in conjunction with models of infectious, autoimmune, and inflammatory diseases. This appears to be the case for both the effects of the endogenous glucocorticoid corticosterone on immune function and the therapeutic effects of glucocorticoid drugs on the disease. When all of these studies are taken into account, it becomes clear that glucocorticoids may target a variety of immune system cells, including innate lymphoid cells, T- and B-cells, myeloid cells (granulocytes, macrophages, and dendritic cells), as well as non-immune cells like epithelial and stromal cells.
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