NDLI: Amelioration of experimental autoimmune encephalomyelitis in IL-4Ralpha-/- mice implicates compensatory up-regulation of Th2-type cytokines.

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Year: 2008 Volume: 172

Year: 2004 Volume: 164

Amelioration of experimental autoimmune encephalomyelitis in IL-4Ralpha-/- mice implicates compensatory up-regulation of Th2-type cytokines.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Gaupp, Stefanie Cannella, Barbara Raine, Cedric S.
Description	Country affiliation: United States Author Affiliation: Gaupp S ( Department of Pathology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.)
Abstract	The cytokine receptor interleukin (IL)-4R, expressed by lymphocytes, is well known for its role in immunomodulatory signaling and has also been documented on oligodendrocytes, suggesting involvement in glial cell interactions. In the present study, we investigated the clinical course and pathology of experimental autoimmune encephalomyelitis in mice demonstrating deletion of IL-4R and found a correlation with cytokine expression during acute and chronic disease. Wild-type (WT) littermates served as controls. Although IL-4R(-/-) mice displayed a milder course throughout, they showed comparable pathology to WT in the acute phase. However, during the chronic phase, IL-4R(-/-) mice exhibited extensive remyelination and an apparent increase in oligodendrocytes. Cytokine patterns were examined by immunocytochemistry, fluorescence-activated cell sorting, and enzyme-linked immunosorbent assay and were strongly proinflammatory within the central nervous system during the acute phase in WT mice whereas IL-4R(-/-) animals expressed higher levels of IL-6 and IL-10 that became more pronounced with time. The milder experimental autoimmune encephalomyelitis and enhanced remyelination in IL-4R(-/-) mice appeared to be related to a shift toward a Th-2 pattern involving mainly IL-6 and IL-10. These data suggest that IL-4R exerts a negative regulatory role on oligodendrocytes that when deleted results in enhanced myelin repair.
File Format	HTM / HTML
ISSN	00029440
e-ISSN	15252191
DOI	10.2353/ajpath.2008.071156
Journal	The American Journal of Pathology
Issue Number	1
Volume Number	173
Language	English
Publisher	Elsevier (on behalf of the American Society for Investigative Pathology)
Publisher Date	2008-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Chemotaxis, Leukocyte Immunohistochemistry Research Support, N.i.h., Extramural Research Support, Non-u.s. Gov't Mice, Inbred Balb C Receptors, Cell Surface Biosynthesis Th2 Cells Interleukin-6 Immunology Flow Cytometry Genetics Interleukin-10 Cytokines Deficiency Discipline Pathology Metabolism Enzyme-linked Immunosorbent Assay Mice, Knockout Encephalomyelitis, Autoimmune, Experimental Pathology Animals Up-regulation Mice
Content Type	Text
Resource Type	Article
Subject	Pathology and Forensic Medicine

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Amelioration of experimental autoimmune encephalomyelitis in IL-4Ralpha-/- mice implicates compensatory up-regulation of Th2-type cytokines.

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Amelioration of experimental autoimmune encephalomyelitis in IL-4Ralpha-/- mice implicates compensatory up-regulation of Th2-type cytokines.