Asset Details
Do you wish to reserve the book?
Central histamine H₃ receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Central histamine H₃ receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS
Do you wish to request the book?
Central histamine H₃ receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Central histamine H₃ receptor signaling negatively regulates susceptibility to autoimmune inflammatory disease of the CNS
2007
Overview
Histamine (HA), a biogenic amine with a broad spectrum of activities in both physiological and pathological settings, plays a key regulatory role in experimental allergic encephalomyelitis, the autoimmune model of multiple sclerosis. HA exerts its effect through four G protein-coupled receptors designated HA receptor H₁, H₂, H₃, and H₄. We report here that, compared with wild-type animals, mice with a disrupted HA H₃ receptor (H3RKO), the expression of which is normally confined to cells of the nervous system, develop more severe disease and neuroinflammation. We show that this effect is associated with dysregulation of blood-brain barrier permeability and increased expression of MIP-2, IP-10, and CXCR3 by peripheral T cells. Our data suggest that pharmacological targeting of the H₃R may be useful in preventing the development and formation of new lesions in multiple sclerosis, thereby significantly limiting the progression of the disease.
Publisher
National Academy of Sciences,National Acad Sciences
Subject
/ Autoimmune diseases of the nervous system
/ Central Nervous System - metabolism
/ Central Nervous System - pathology
/ Central nervous system diseases
/ Disease Susceptibility - immunology
/ Encephalomyelitis, Autoimmune, Experimental - immunology
/ Encephalomyelitis, Autoimmune, Experimental - pathology
/ hydrogen
/ Lesions
/ Mice
/ Neurons
