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Chemokine expression in murine experimental allergic encephalomyelitis
R Godiska1, D Chantry, G N Dietsch
1ICOS Corporation, Bothell, WA 98021, USA.
Journal of Neuroimmunology
|May 1, 1995
Summary
Chemokines, proteins involved in cell signaling, are upregulated in the spinal cord during experimental allergic encephalomyelitis (EAE), a model for multiple sclerosis. This suggests specific chemokines play a key role in this autoimmune disease.
Area of Science:
- Immunology
- Neuroscience
- Molecular Biology
Background:
- Chemokines are low molecular mass proteins mediating chemotactic and cell-activating activities.
- Experimental allergic encephalomyelitis (EAE) in mice serves as a crucial model for studying multiple sclerosis (MS).
Purpose of the Study:
- To investigate the expression patterns of various chemokines during the development of murine EAE.
- To identify specific chemokines involved in the inflammatory processes of EAE.
Main Methods:
- Utilized reverse transcription-polymerase chain reaction (RT-PCR) and Northern hybridization.
- Examined gene expression in spinal cord tissues from mice with EAE.
Main Results:
- Induced mRNA expression of RANTES, MIP-1 alpha, MIP-1 beta, TCA3, IP-10, JE (MCP-1), KC (MGSA/gro), and MARC (MCP-3) in the spinal cord prior to clinical EAE onset.
- SDF, a chemokine-like product, was expressed in both normal and diseased spinal cords.
- Activated encephalitogenic T cells expressed RANTES, MIP-1 alpha, MIP-1 beta, and TCA3.
Conclusions:
- A specific subset of chemokines is significantly upregulated during EAE.
- These identified chemokines likely contribute to the inflammatory pathology observed in EAE and potentially in MS.