Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 104, Issue 24, Pages 10146-10151Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.0702291104
Keywords
blood-brain barrier; experimental allergic encephalomyelitis; multiple sclerosis
Categories
Funding
- NIAID NIH HHS [AI 058052, AI 045666, R01 AI058052, AI 041747, P01 AI045666, R01 AI041747] Funding Source: Medline
- NINDS NIH HHS [R01 NS036526, NS 036526] Funding Source: Medline
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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 H-1, H-2, H-3, and H-4. We report here that, compared with wild-type animals, mice with a disrupted HA H-3 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.
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