Journal
JOURNAL OF IMMUNOLOGY
Volume 184, Issue 12, Pages 6891-6900Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1000126
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Funding
- National Multiple Sclerosis Society [RG3104B3]
- National Institutes of Health [NS047578, F31 NS054395]
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Mast cells contribute to the pathogenesis of experimental autoimmune encephalomyelitis, a rodent model of the human demyelinating disease multiple sclerosis. Yet their site and mode of action is unknown. In both diseases, myelin-specific T cells are initially activated in peripheral lymphoid organs. However, for disease to occur, these cells must enter the immunologically privileged CNS through a breach in the relatively impermeable blood-brain barrier. In this study, we demonstrate that a dense population of resident mast cells in the meninges, structures surrounding the brain and spinal cord, regulate basal CNS barrier function, facilitating initial T cell CNS entry. Through the expression of TNF, mast cells recruit an early wave of neutrophils to the CNS. We propose that neutrophils in turn promote the blood-brain barrier breach and together with T cells lead to further inflammatory cell influx and myelin damage. These findings provide specific targets for intervention in multiple sclerosis as well as other immune-mediated CNS diseases. The Journal of Immunology, 2010, 184: 6891-6900.
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