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      The leukotriene B4 receptor, BLT1, is required for the induction of experimental autoimmune encephalomyelitis.

      Biochemical and Biophysical Research Communications

      Amino Acid Sequence, Animals, Cell Movement, immunology, Encephalomyelitis, Autoimmune, Experimental, genetics, metabolism, pathology, Mice, Mice, Inbred C57BL, Mice, Knockout, Molecular Sequence Data, Receptors, Leukotriene B4, Spinal Cord, Th1 Cells, Th2 Cells

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          Abstract

          Leukotriene B(4) (LTB(4)) is a potent chemoattractant and activator of neutrophils, macrophages and T cells. These cells are a key component of inflammation and all express BLT1, a high affinity G-protein-coupled receptor for LTB(4). However, little is known about the neuroimmune functions of BLT1. In this study, we describe a distinct role for BLT1 in the pathology of experimental autoimmune encephalomyelitis (EAE) and T(H)1/T(H)17 immune responses. BLT1 mRNA was highly upregulated in the spinal cord of EAE mice, especially during the induction phase. BLT1(-/-) mice had delayed onset and less severe symptoms of EAE than BLT1(+/+) mice. Additionally, inflammatory cells were recruited to the spinal cord of asymptomatic BLT1(+/+), but not BLT1(-/-) mice before the onset of disease. Ex vivo studies showed that both the proliferation and the production of IFN-gamma, TNF-alpha, IL-17 and IL-6 were impaired in BLT1(-/-) cells, as compared with BLT1(+/+) cells. Thus, we suggest that BLT1 exacerbates EAE by regulating the migration of inflammatory cells and T(H)1/T(H)17 immune responses. Our findings provide a novel therapeutic option for the treatment of multiple sclerosis and other T(H)17-mediated diseases. Copyright 2010 Elsevier Inc. All rights reserved.

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          Journal
          20226760
          10.1016/j.bbrc.2010.03.049

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