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Effects of cytokine deficiency on chemokine expression in CNS of mice with EAE.
J Neurosci Res. 2002 Mar 01; 67(5):680-8.JN

Abstract

Although both cytokines and chemokines have been implicated in the pathogenesis of clinical and histological EAE, their interactions in vivo have not yet been clearly established. To address this issue, we evaluated expression of chemokines and receptors in the CNS of wild-type control and cytokine deficient mice at the peak of EAE induced with MOG-35-55 peptide in CFA. Our results demonstrate that: 1) expression of most chemokines/receptors was drastically inhibited in TNF-alpha deficient mice, and was reflective of delayed onset and reduced severity of EAE; 2) distinct patterns of chemokine expression occurred in various other cytokine knockout mice that did not significantly affect expression of clinical EAE; 3) there was a strong association between expression of MIP-1alpha, MIP-2 and MCP-1 in CNS and overall severity of EAE in wild-type and cytokine knockout mice; and 4) among CNS infiltrating cells at the peak of EAE, macrophages and CD8+ T cells were the primary cellular source of most of the chemokines. Of note, we present evidence that TNF-alpha may be involved in regulating RANTES and MIP-1alpha, and that IL-4 may be involved in regulating MCP-1. Our results not only identify the cellular source of chemokines in CNS, but also implicate MIP-1alpha, MIP-2, and MCP-1 in controlling CNS inflammation and severity of EAE.

Authors+Show Affiliations

Department of Neurology, Oregon Health and Science University, Portland, Oregon, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Research Support, U.S. Gov't, P.H.S.

Language

eng

PubMed ID

11891780

Citation

Matejuk, Agata, et al. "Effects of Cytokine Deficiency On Chemokine Expression in CNS of Mice With EAE." Journal of Neuroscience Research, vol. 67, no. 5, 2002, pp. 680-8.
Matejuk A, Dwyer J, Ito A, et al. Effects of cytokine deficiency on chemokine expression in CNS of mice with EAE. J Neurosci Res. 2002;67(5):680-8.
Matejuk, A., Dwyer, J., Ito, A., Bruender, Z., Vandenbark, A. A., & Offner, H. (2002). Effects of cytokine deficiency on chemokine expression in CNS of mice with EAE. Journal of Neuroscience Research, 67(5), 680-8.
Matejuk A, et al. Effects of Cytokine Deficiency On Chemokine Expression in CNS of Mice With EAE. J Neurosci Res. 2002 Mar 1;67(5):680-8. PubMed PMID: 11891780.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effects of cytokine deficiency on chemokine expression in CNS of mice with EAE. AU - Matejuk,Agata, AU - Dwyer,Jami, AU - Ito,Atsushi, AU - Bruender,Zachary, AU - Vandenbark,Arthur A, AU - Offner,Halina, PY - 2002/3/14/pubmed PY - 2002/5/1/medline PY - 2002/3/14/entrez SP - 680 EP - 8 JF - Journal of neuroscience research JO - J Neurosci Res VL - 67 IS - 5 N2 - Although both cytokines and chemokines have been implicated in the pathogenesis of clinical and histological EAE, their interactions in vivo have not yet been clearly established. To address this issue, we evaluated expression of chemokines and receptors in the CNS of wild-type control and cytokine deficient mice at the peak of EAE induced with MOG-35-55 peptide in CFA. Our results demonstrate that: 1) expression of most chemokines/receptors was drastically inhibited in TNF-alpha deficient mice, and was reflective of delayed onset and reduced severity of EAE; 2) distinct patterns of chemokine expression occurred in various other cytokine knockout mice that did not significantly affect expression of clinical EAE; 3) there was a strong association between expression of MIP-1alpha, MIP-2 and MCP-1 in CNS and overall severity of EAE in wild-type and cytokine knockout mice; and 4) among CNS infiltrating cells at the peak of EAE, macrophages and CD8+ T cells were the primary cellular source of most of the chemokines. Of note, we present evidence that TNF-alpha may be involved in regulating RANTES and MIP-1alpha, and that IL-4 may be involved in regulating MCP-1. Our results not only identify the cellular source of chemokines in CNS, but also implicate MIP-1alpha, MIP-2, and MCP-1 in controlling CNS inflammation and severity of EAE. SN - 0360-4012 UR - https://www.unboundmedicine.com/medline/citation/11891780/Effects_of_cytokine_deficiency_on_chemokine_expression_in_CNS_of_mice_with_EAE_ L2 - https://doi.org/10.1002/jnr.10156 DB - PRIME DP - Unbound Medicine ER -