title: Toll-like receptors in endocrine disease and diabetes.
abstract: The body's ability to keep a steady homeostatic state is crucial to health and life. This involves providing an adequate response to a variety of challenges both physical and mental, such as microbial invasion and emotional distress. Interplay between the neuroendocrine and immune systems is essential in either case. Studies have demonstrated that toll-like receptors, or TLRs, play a regulatory role in both systems, and have been proposed as a possible link between the immune, hormonal and metabolic systems. As part of the innate immune system, these receptors control the identification by the body of microbial invaders and its immediate reaction in immune and inflammatory response. What are referred to as pattern recognition receptors are mostly expressed by cells involved in hematopoietic linkage, but an increasing number of studies have demonstrated their expression in other cell types such as neurons and endocrine cells on the hypothalamic-pituitary-adrenal (HPA) axis, thyrocytes, adipocytes and islets of Langerhans. Together with endocrine and metabolic dysregulation, immune system overreaction is often associated with infection and autoimmunity, clearly indicating TLR involvement at organ level which affects organ function. Several diseases such as autoimmune thyroid and pancreatic diseases, septic dysregulation of the HPA axis, diabetes and the metabolic syndrome have been linked to TLR activation and polymorphism. To gain insight into stress response and adaptation, we need to know more about TLRs and the specific physiological role they play in the endocrine and metabolic system and its processes.
authors.affiliation: Department of Medicine III, Carl Gustav Carus University Hospital, Dresden, Germany.
authors.forename: W
authors.initials: W
authors.lastname: Kanczkowski
authors.forename: C G
authors.initials: CG
authors.lastname: Ziegler
authors.forename: K
authors.initials: K
authors.lastname: Zacharowski
authors.forename: S R
authors.initials: SR
authors.lastname: Bornstein
mesh_terms: D000818:Animals; D001327:Autoimmune Diseases / Q000276:immunology* / Q000503:physiopathology; D003920:Diabetes Mellitus / Q000276:immunology* / Q000503:physiopathology; D004700:Endocrine System Diseases / Q000276:immunology* / Q000503:physiopathology; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000276:immunology / Q000503:physiopathology; D024821:Metabolic Syndrome / Q000276:immunology / Q000503:physiopathology; D009490:Neurosecretory Systems / Q000276:immunology* / Q000503:physiopathology; D051193:Toll-Like Receptors / Q000276:immunology*
chemical_list: D051193:Toll-Like Receptors