Induction of experimental autoimmune encephalomyelitis in C57BL/6 mice deficient in either the chemokine macrophage inflammatory protein-1alpha or its CCR5 receptor.

E H Tran, W A Kuziel, T Owens

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

Resumé

Udgivelsesdato: 2000-May
OriginalsprogEngelsk
TidsskriftEuropean Journal of Immunology
Vol/bind30
Udgave nummer5
Sider (fra-til)1410-5
Antal sider5
ISSN0014-2980
StatusUdgivet - 1. maj 2000

Fingeraftryk

CCR5 Receptors
Autoimmune Experimental Encephalomyelitis
Macrophages
Chemokine CXCL10
Chemokine CCL5
Blocking Antibodies
Central Nervous System Diseases
Ribonucleases
Transcriptional Activation
Pathology
Messenger RNA

Citer dette

@article{9109b8d04c2411ddb1a1000ea68e967b,
title = "Induction of experimental autoimmune encephalomyelitis in C57BL/6 mice deficient in either the chemokine macrophage inflammatory protein-1alpha or its CCR5 receptor.",
abstract = "Macrophage inflammatory protein (MIP)-1alpha is a chemokine that is associated with Th1 cytokine responses. Expression and antibody blocking studies have implicated MIP-1alpha in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). We examined the role of MIP-1alpha and its CCR5 receptor in the induction of EAE by immunizing C57BL / 6 mice deficient in either MIP-1alpha or CCR5 with myelin oligodendrocyte glycoprotein (MOG). We found that MIP-1alpha-deficient mice were fully susceptible to MOG-induced EAE. These knockout animals were indistinguishable from wild-type mice in Th1 cytokine gene expression, the kinetics and severity of disease, and infiltration of the central nervous system by lymphocytes, macrophages and granulocytes. RNase protection assays showed comparable accumulation of mRNA for the chemokines interferon-inducible protein-10, RANTES, macrophage chemoattractant protein-1, MIP-1beta, MIP-2, lymphotactin and T cell activation gene-3 during the course of the disease. CCR5-deficient mice were also susceptible to disease induction by MOG. The dispensability of MIP-1alpha and CCR5 for MOG-induced EAE in C57BL / 6 mice supports the idea that differential chemokine expression patterns represent differences in disease mechanism that underlie various models of EAE, and possibly distinct patterns of pathology seen in MS.",
keywords = "Animals, Autoimmunity, Chemokine CCL3, Chemokine CCL4, Encephalomyelitis, Autoimmune, Experimental, Lymphocyte Activation, Macrophage Inflammatory Proteins, Mice, Mice, Inbred C57BL, Receptors, CCR5, T-Lymphocytes",
author = "Tran, {E H} and Kuziel, {W A} and T Owens",
year = "2000",
month = "5",
day = "1",
language = "English",
volume = "30",
pages = "1410--5",
journal = "European Journal of Immunology",
issn = "0014-2980",
publisher = "Wiley - V C H Verlag GmbH & Co. KGaA",
number = "5",

}

Induction of experimental autoimmune encephalomyelitis in C57BL/6 mice deficient in either the chemokine macrophage inflammatory protein-1alpha or its CCR5 receptor. / Tran, E H; Kuziel, W A; Owens, T.

I: European Journal of Immunology, Bind 30, Nr. 5, 01.05.2000, s. 1410-5.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

TY - JOUR

T1 - Induction of experimental autoimmune encephalomyelitis in C57BL/6 mice deficient in either the chemokine macrophage inflammatory protein-1alpha or its CCR5 receptor.

AU - Tran, E H

AU - Kuziel, W A

AU - Owens, T

PY - 2000/5/1

Y1 - 2000/5/1

N2 - Macrophage inflammatory protein (MIP)-1alpha is a chemokine that is associated with Th1 cytokine responses. Expression and antibody blocking studies have implicated MIP-1alpha in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). We examined the role of MIP-1alpha and its CCR5 receptor in the induction of EAE by immunizing C57BL / 6 mice deficient in either MIP-1alpha or CCR5 with myelin oligodendrocyte glycoprotein (MOG). We found that MIP-1alpha-deficient mice were fully susceptible to MOG-induced EAE. These knockout animals were indistinguishable from wild-type mice in Th1 cytokine gene expression, the kinetics and severity of disease, and infiltration of the central nervous system by lymphocytes, macrophages and granulocytes. RNase protection assays showed comparable accumulation of mRNA for the chemokines interferon-inducible protein-10, RANTES, macrophage chemoattractant protein-1, MIP-1beta, MIP-2, lymphotactin and T cell activation gene-3 during the course of the disease. CCR5-deficient mice were also susceptible to disease induction by MOG. The dispensability of MIP-1alpha and CCR5 for MOG-induced EAE in C57BL / 6 mice supports the idea that differential chemokine expression patterns represent differences in disease mechanism that underlie various models of EAE, and possibly distinct patterns of pathology seen in MS.

AB - Macrophage inflammatory protein (MIP)-1alpha is a chemokine that is associated with Th1 cytokine responses. Expression and antibody blocking studies have implicated MIP-1alpha in multiple sclerosis (MS) and in experimental autoimmune encephalomyelitis (EAE). We examined the role of MIP-1alpha and its CCR5 receptor in the induction of EAE by immunizing C57BL / 6 mice deficient in either MIP-1alpha or CCR5 with myelin oligodendrocyte glycoprotein (MOG). We found that MIP-1alpha-deficient mice were fully susceptible to MOG-induced EAE. These knockout animals were indistinguishable from wild-type mice in Th1 cytokine gene expression, the kinetics and severity of disease, and infiltration of the central nervous system by lymphocytes, macrophages and granulocytes. RNase protection assays showed comparable accumulation of mRNA for the chemokines interferon-inducible protein-10, RANTES, macrophage chemoattractant protein-1, MIP-1beta, MIP-2, lymphotactin and T cell activation gene-3 during the course of the disease. CCR5-deficient mice were also susceptible to disease induction by MOG. The dispensability of MIP-1alpha and CCR5 for MOG-induced EAE in C57BL / 6 mice supports the idea that differential chemokine expression patterns represent differences in disease mechanism that underlie various models of EAE, and possibly distinct patterns of pathology seen in MS.

KW - Animals

KW - Autoimmunity

KW - Chemokine CCL3

KW - Chemokine CCL4

KW - Encephalomyelitis, Autoimmune, Experimental

KW - Lymphocyte Activation

KW - Macrophage Inflammatory Proteins

KW - Mice

KW - Mice, Inbred C57BL

KW - Receptors, CCR5

KW - T-Lymphocytes

M3 - Journal article

C2 - 10820388

VL - 30

SP - 1410

EP - 1415

JO - European Journal of Immunology

JF - European Journal of Immunology

SN - 0014-2980

IS - 5

ER -