Journal
CLINICAL IMMUNOLOGY
Volume 189, Issue -, Pages 14-22Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.clim.2016.04.009
Keywords
Mast cells; Meninges; EAE; Multiple sclerosis; CNS demyelinating disease; Inflammasome; T cell pathogenicity; GM-CSF; IL-1 beta
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Funding
- NIGMS NIH HHS [T32 GM008152] Funding Source: Medline
- NINDS NIH HHS [F31 NS084691] Funding Source: Medline
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Inflammasomes are multiprotein complexes that assemble in response to microbial and other danger signals and regulate the secretion of biologically active IL-1 beta and IL-18. Although they are important in protective immunity against bacterial, viral and parasitic infections, aberrant inflammasome activity promotes chronic inflammation associated with autoimmune disease. Inflammasomes have been described in many immune cells, but the majority of studies have focused on their activity in macrophages. Here we discuss an important role for mast cell-inflammasome activity in EAE, the rodent model of multiple sclerosis, a CNS demyelinating disease. We review our evidence that mast cells in the meninges, tissues that surround the brain and spinal cord, interact with infiltrating myelin-specific T cells in early disease. This interaction elicits IL-1 beta expression by mast cells, which in turn, promotes GM-CSF expression by T cells. In view of the essential role that GM-CSF plays in T cell encephalitogenicity, we propose this mast cell-T cell crosstalk in the meninges is critical for EAE disease development. (C) 2016 Elsevier Inc. All rights reserved.
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