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Modulation of experimental autoimmune encephalomyelitis: effect of altered peptide ligand on chemokine and chemokine receptor expression.
J Neuroimmunol. 2000 Oct 02; 110(1-2):195-208.JN

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a T helper 1 (Th1) cell mediated demyelinating disease and the principal animal model for multiple sclerosis. Spinal cords from SJL mice primed with proteolipid protein peptide 139-151 (pPLP) expressed the chemokines RANTES, MCP-1, MIP-2, KC, MIP-1alpha, MIP-1beta, Mig, and fractalkine. We also identified IP-10 in these samples and described a sequence polymorphism in this transcript. Chemokine expression was specific for tissues of the central nervous system. MCP-1, IP-10, and MIP-2 RNA expression significantly correlated with clinical score. Chemokine receptor expression generally correlated with ligand expression. pPLP-primed mice expressed the Th1-associated markers CCR5 and CXCR3 on mononuclear cells. In addition, cells expressing CCR1, CCR2, CCR3, CCR4, CCR8, and CXCR2 were detected. Here we demonstrate that altered peptide ligand (APL)-induced protection from EAE was accompanied by modulation of chemokine and chemokine receptor expression. Spinal cord tissue sections from APL-protected mice showed greatly reduced levels of all chemokines and of CCR1, CCR5, CCR8, CXCR2 and CXCR3. The Th2-associated chemokine receptors CCR3 and CCR4 were found in protected mice, supporting the hypothesis that Th1 but not Th2 cells are down-regulated by APL treatment. This report concludes that chemokines and chemokine receptors can be useful tools to follow modulation of autoimmune disease.

Authors+Show Affiliations

Department of Pathology, Harvard Medical School, 200 Longwood Ave, Boston, MA 02115, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

11024550

Citation

Fischer, F R., et al. "Modulation of Experimental Autoimmune Encephalomyelitis: Effect of Altered Peptide Ligand On Chemokine and Chemokine Receptor Expression." Journal of Neuroimmunology, vol. 110, no. 1-2, 2000, pp. 195-208.
Fischer FR, Santambrogio L, Luo Y, et al. Modulation of experimental autoimmune encephalomyelitis: effect of altered peptide ligand on chemokine and chemokine receptor expression. J Neuroimmunol. 2000;110(1-2):195-208.
Fischer, F. R., Santambrogio, L., Luo, Y., Berman, M. A., Hancock, W. W., & Dorf, M. E. (2000). Modulation of experimental autoimmune encephalomyelitis: effect of altered peptide ligand on chemokine and chemokine receptor expression. Journal of Neuroimmunology, 110(1-2), 195-208.
Fischer FR, et al. Modulation of Experimental Autoimmune Encephalomyelitis: Effect of Altered Peptide Ligand On Chemokine and Chemokine Receptor Expression. J Neuroimmunol. 2000 Oct 2;110(1-2):195-208. PubMed PMID: 11024550.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Modulation of experimental autoimmune encephalomyelitis: effect of altered peptide ligand on chemokine and chemokine receptor expression. AU - Fischer,F R, AU - Santambrogio,L, AU - Luo,Y, AU - Berman,M A, AU - Hancock,W W, AU - Dorf,M E, PY - 2000/10/12/pubmed PY - 2001/2/28/medline PY - 2000/10/12/entrez SP - 195 EP - 208 JF - Journal of neuroimmunology JO - J Neuroimmunol VL - 110 IS - 1-2 N2 - Experimental autoimmune encephalomyelitis (EAE) is a T helper 1 (Th1) cell mediated demyelinating disease and the principal animal model for multiple sclerosis. Spinal cords from SJL mice primed with proteolipid protein peptide 139-151 (pPLP) expressed the chemokines RANTES, MCP-1, MIP-2, KC, MIP-1alpha, MIP-1beta, Mig, and fractalkine. We also identified IP-10 in these samples and described a sequence polymorphism in this transcript. Chemokine expression was specific for tissues of the central nervous system. MCP-1, IP-10, and MIP-2 RNA expression significantly correlated with clinical score. Chemokine receptor expression generally correlated with ligand expression. pPLP-primed mice expressed the Th1-associated markers CCR5 and CXCR3 on mononuclear cells. In addition, cells expressing CCR1, CCR2, CCR3, CCR4, CCR8, and CXCR2 were detected. Here we demonstrate that altered peptide ligand (APL)-induced protection from EAE was accompanied by modulation of chemokine and chemokine receptor expression. Spinal cord tissue sections from APL-protected mice showed greatly reduced levels of all chemokines and of CCR1, CCR5, CCR8, CXCR2 and CXCR3. The Th2-associated chemokine receptors CCR3 and CCR4 were found in protected mice, supporting the hypothesis that Th1 but not Th2 cells are down-regulated by APL treatment. This report concludes that chemokines and chemokine receptors can be useful tools to follow modulation of autoimmune disease. SN - 0165-5728 UR - https://www.unboundmedicine.com/medline/citation/11024550/Modulation_of_experimental_autoimmune_encephalomyelitis:_effect_of_altered_peptide_ligand_on_chemokine_and_chemokine_receptor_expression_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0165-5728(00)00351-9 DB - PRIME DP - Unbound Medicine ER -