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Sialoadhesin deficiency ameliorates myelin degeneration and axonopathic changes in the CNS of PLP overexpressing mice. Neurobiol Dis 2007 Jan;25(1):105-11

Date

10/27/2006

Pubmed ID

17064921

DOI

10.1016/j.nbd.2006.08.023

Scopus ID

2-s2.0-33751102165   45 Citations

Abstract

PLP overexpressing mice display demyelination and axonopathic changes, accompanied by an elevation of CD8+ T-lymphocytes and CD11b+ macrophages in the CNS. By crossbreeding these mutants with RAG-1-deficient mice lacking mature lymphocytes, we could recently demonstrate a pathogenetic impact of the CD8+ cells. In the present study, we investigated the pathogenetic impact of CD11b+ macrophages by crossbreeding the myelin mutants with knockout mice deficient for the macrophage-restricted adhesion molecule sialoadhesin (Sn). In the wild-type mice, Sn is barely detectable on CD11b+ cells, whereas in the myelin mutants, almost all CD11b+ cells express Sn. In the double mutants, upregulation of CD8+ T-cells and CD11b+ macrophages is reduced and pathological alterations are ameliorated. These data indicate that in a primarily genetically caused myelin disorder of the CNS macrophages expressing Sn partially mediate pathogenesis. These findings may have substantial impact on treatment strategies for leukodystrophic disorders and some forms of multiple sclerosis.

Author List

Ip CW, Kroner A, Crocker PR, Nave KA, Martini R

Author

Antje Kroner-Milsch MD, PhD Assistant Professor in the Neurosurgery department at Medical College of Wisconsin




MESH terms used to index this publication - Major topics in bold

Animals
Axons
CD11b Antigen
CD8-Positive T-Lymphocytes
Central Nervous System
Genotype
Immunohistochemistry
Macrophages
Membrane Glycoproteins
Mice
Mice, Inbred C57BL
Mice, Transgenic
Microscopy, Electron
Myelin Sheath
Phospholipases
Receptors, Immunologic
Sialic Acid Binding Ig-like Lectin 1