In:
The Journal of Immunology, The American Association of Immunologists, Vol. 182, No. 1_Supplement ( 2009-04-01), p. 50.2-50.2
Abstract:
We attempted to understand the immune modulation mediated by chondroitin sulfate A (CS-A) and its disaccharide degradation product (CSPG-DS) in the development of experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Clinical symptoms in myelin oligodendrocyte glycoprotein peptide (MOG35-55)-induced EAE mice significantly enhanced following CS-A injection, whereas CSPG-DS injection completely inhibited EAE development. When a clinically more severe form of EAE was induced, CS-A accelerated the clinical disease, whereas CSPG-DS significantly delayed EAE. Further studies demonstrated that CS-A up-regulated STAT4 expression, and thus induced interferon-gamma production and Th1 CD4 T cell differentiation. CS-A also up-regulated STAT3 expression and increased IL-17 producing T cell populations. CSPG-DS treatment both in vivo and in vitro decreased tumor necrosis factor - alpha production from splenocytes. In vitro and in vivo assay indicated that CSPG-DS treatment significantly blocked T cell migration, whereas CS-A treatment increased lymphocyte infiltration in the brain when compared to MOG-treated control mice. Our results suggest that while CS-A exacerbates the development of EAE, CSPG-DS administration may be useful in its treatment. (Supported in part by NIH grants R01AI053703, R01ES09098, R01 AI058300, R01DA016545, R01HL058641 and P01AT003961).
Type of Medium:
Online Resource
ISSN:
0022-1767
,
1550-6606
DOI:
10.4049/jimmunol.182.Supp.50.2
Language:
English
Publisher:
The American Association of Immunologists
Publication Date:
2009
detail.hit.zdb_id:
1475085-5
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