Region-specific regulation of inflammation and pathogenesis in experimental autoimmune encephalomyelitis

Angela S. Archambault; Julia Sim; Erin E. McCandless; Robyn S. Klein; John H. Russell

doi:10.1016/j.jneuroim.2006.08.012

Region-specific regulation of inflammation and pathogenesis in experimental autoimmune encephalomyelitis

Angela S. Archambault, Julia Sim, Erin E. McCandless, Robyn S. Klein, John H. Russell

Research output: Contribution to journal › Article › peer-review

23 Scopus citations

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis and is characterized by an infiltrate of predominately T cells and macrophages in the spinal cord and brain. In both the spinal cord and the cerebellum, Th1 cells direct inflammation to antigen-rich white matter tracts, and there is a TNFR1-dependent recruitment of CD11b^hi cells in both regions. In the spinal cord, parenchymal invasion, demyelination and clinical symptoms are associated with TNFR1-dependant parenchymal induction (especially astrocytes) of VCAM-1 and CXCL2. None of these events occur in the cerebellum despite the fact that an inflammatory infiltrate accumulates in the perivascular space. Therefore regional specificity in astrocyte responses to inflammatory cytokines may regulate regional parenchymal infiltration and pathogenesis.

Original language	English
Pages (from-to)	122-132
Number of pages	11
Journal	Journal of Neuroimmunology
Volume	181
Issue number	1-2
DOIs	https://doi.org/10.1016/j.jneuroim.2006.08.012
State	Published - Dec 2006

Keywords

Cerebellum
Chemokines
Experimental autoimmune encephalomyelitis
T cells
VCAM-1

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10.1016/j.jneuroim.2006.08.012

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title = "Region-specific regulation of inflammation and pathogenesis in experimental autoimmune encephalomyelitis",

abstract = "Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis and is characterized by an infiltrate of predominately T cells and macrophages in the spinal cord and brain. In both the spinal cord and the cerebellum, Th1 cells direct inflammation to antigen-rich white matter tracts, and there is a TNFR1-dependent recruitment of CD11bhi cells in both regions. In the spinal cord, parenchymal invasion, demyelination and clinical symptoms are associated with TNFR1-dependant parenchymal induction (especially astrocytes) of VCAM-1 and CXCL2. None of these events occur in the cerebellum despite the fact that an inflammatory infiltrate accumulates in the perivascular space. Therefore regional specificity in astrocyte responses to inflammatory cytokines may regulate regional parenchymal infiltration and pathogenesis.",

keywords = "Cerebellum, Chemokines, Experimental autoimmune encephalomyelitis, T cells, VCAM-1",

author = "Archambault, {Angela S.} and Julia Sim and McCandless, {Erin E.} and Klein, {Robyn S.} and Russell, {John H.}",

note = "Funding Information: The authors thank Kira Moore for technical assistance and Dr. Jason Lees for a critical discussion of the manuscript. This work was supported by grants from the National Institutes of Health (NS045607, R.S.K.), and the National Multiple Sclerosis Society (RG 3314 and 3732, J.H.R.; RG 3450, R.S.K.).",

year = "2006",

month = dec,

doi = "10.1016/j.jneuroim.2006.08.012",

language = "English",

volume = "181",

pages = "122--132",

journal = "Journal of Neuroimmunology",

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T1 - Region-specific regulation of inflammation and pathogenesis in experimental autoimmune encephalomyelitis

AU - Archambault, Angela S.

AU - Sim, Julia

AU - McCandless, Erin E.

AU - Klein, Robyn S.

AU - Russell, John H.

N1 - Funding Information: The authors thank Kira Moore for technical assistance and Dr. Jason Lees for a critical discussion of the manuscript. This work was supported by grants from the National Institutes of Health (NS045607, R.S.K.), and the National Multiple Sclerosis Society (RG 3314 and 3732, J.H.R.; RG 3450, R.S.K.).

PY - 2006/12

Y1 - 2006/12

N2 - Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis and is characterized by an infiltrate of predominately T cells and macrophages in the spinal cord and brain. In both the spinal cord and the cerebellum, Th1 cells direct inflammation to antigen-rich white matter tracts, and there is a TNFR1-dependent recruitment of CD11bhi cells in both regions. In the spinal cord, parenchymal invasion, demyelination and clinical symptoms are associated with TNFR1-dependant parenchymal induction (especially astrocytes) of VCAM-1 and CXCL2. None of these events occur in the cerebellum despite the fact that an inflammatory infiltrate accumulates in the perivascular space. Therefore regional specificity in astrocyte responses to inflammatory cytokines may regulate regional parenchymal infiltration and pathogenesis.

AB - Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis and is characterized by an infiltrate of predominately T cells and macrophages in the spinal cord and brain. In both the spinal cord and the cerebellum, Th1 cells direct inflammation to antigen-rich white matter tracts, and there is a TNFR1-dependent recruitment of CD11bhi cells in both regions. In the spinal cord, parenchymal invasion, demyelination and clinical symptoms are associated with TNFR1-dependant parenchymal induction (especially astrocytes) of VCAM-1 and CXCL2. None of these events occur in the cerebellum despite the fact that an inflammatory infiltrate accumulates in the perivascular space. Therefore regional specificity in astrocyte responses to inflammatory cytokines may regulate regional parenchymal infiltration and pathogenesis.

KW - Cerebellum

KW - Chemokines

KW - Experimental autoimmune encephalomyelitis

KW - T cells

KW - VCAM-1

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U2 - 10.1016/j.jneuroim.2006.08.012

DO - 10.1016/j.jneuroim.2006.08.012

M3 - Article

C2 - 17030428

AN - SCOPUS:33751515069

SN - 0165-5728

VL - 181

SP - 122

EP - 132

JO - Journal of Neuroimmunology

JF - Journal of Neuroimmunology

IS - 1-2

ER -

Region-specific regulation of inflammation and pathogenesis in experimental autoimmune encephalomyelitis

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Keywords

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