Institute of Biomedical Sciences

Title

The role of B cells in modulating microglial activation in EAE

Poster Number

19

Document Type

Poster

Status

Graduate Student - Doctoral

Abstract Category

Neuroscience

Keywords

B cell, microglia, EAE, multiple sclerosis

Publication Date

Spring 2018

Abstract

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination, blood-brain barrier dysfunction, and focal areas of inflammation. During disease, there is an influx of peripheral immune cells such as B cells that is accompanied by an activation and proliferation of microglial cells in the CNS, exacerbating the neuroinflammation. B cell depletion therapy efficiently reduces MS relapses, suggesting that B cells play a central role in MS. The precise role of B cells in modulating disease including propagating microglia induced inflammation and neurodegeneration remains unclear. In the current study, we induce experimental autoimmune encephalomyelitis (EAE), an animal model for MS, to investigate microglial activation and B cell infiltration in the mouse spinal cord. Subcutaneous injection of myelin oligodendrocyte glycoprotein induces EAE, and we have examined microglial activation and B cell infiltration using Iba1 and CD19 immunostaining in this model. In addition, we have analyzed pro-inflammatory cytokine levels produced by microglial cells in response to activated B cells in vitro. Induction of EAE leads to inflammation in the spinal cord, quantified by increased Iba1+ cells. Activated B cells modulate the inflammatory response of microglial cells through secretion of pro-and anti-inflammatory cytokines, suggesting that B cells can influence the pathological pathways. Together, these results indicate a potential disease-relevant interaction between infiltrating B cells and resident microglia in the CNS, which may influence the propagation of MS-related inflammation.

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Creative Commons License
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The role of B cells in modulating microglial activation in EAE

Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination, blood-brain barrier dysfunction, and focal areas of inflammation. During disease, there is an influx of peripheral immune cells such as B cells that is accompanied by an activation and proliferation of microglial cells in the CNS, exacerbating the neuroinflammation. B cell depletion therapy efficiently reduces MS relapses, suggesting that B cells play a central role in MS. The precise role of B cells in modulating disease including propagating microglia induced inflammation and neurodegeneration remains unclear. In the current study, we induce experimental autoimmune encephalomyelitis (EAE), an animal model for MS, to investigate microglial activation and B cell infiltration in the mouse spinal cord. Subcutaneous injection of myelin oligodendrocyte glycoprotein induces EAE, and we have examined microglial activation and B cell infiltration using Iba1 and CD19 immunostaining in this model. In addition, we have analyzed pro-inflammatory cytokine levels produced by microglial cells in response to activated B cells in vitro. Induction of EAE leads to inflammation in the spinal cord, quantified by increased Iba1+ cells. Activated B cells modulate the inflammatory response of microglial cells through secretion of pro-and anti-inflammatory cytokines, suggesting that B cells can influence the pathological pathways. Together, these results indicate a potential disease-relevant interaction between infiltrating B cells and resident microglia in the CNS, which may influence the propagation of MS-related inflammation.