Suppression of experimental autoimmune myasthenia gravis by inhibiting the signaling between IFN-gamma inducible protein 10 (IP-10) and its receptor CXCR3.

Authors: Feferman, T  Aricha, R  Mizrachi, K  Geron, E  Alon, R  Souroujon, MC  Fuchs, S 
Citation: Feferman T, etal., J Neuroimmunol. 2009 Apr 30;209(1-2):87-95. Epub 2009 Feb 20.
Pubmed: (View Article at PubMed) PMID:19232748
DOI: Full-text: DOI:10.1016/j.jneuroim.2009.01.021

We have previously demonstrated that the chemokine IFN-gamma inducible protein 10 (IP-10) and its receptor CXCR3, are overexpressed in myasthenia gravis (MG) and its animal model experimental autoimmune MG (EAMG). We now studied the potential of modulating rat EAMG by interference in CXCR3/IP-10 signaling. Two different approaches were used: 1) blocking IP-10 by IP-10-specific antibodies and 2) inhibiting the CXCR3 chemokine receptor by a CXCR3 antagonist. Treatment by either of these reagents led to suppression of EAMG suggesting that inhibition of CXCR3/IP-10 signaling can be considered as a potential treatment modality for MG.


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CRRD Object Information
CRRD ID: 2311364
Created: 2009-07-08
Species: All species
Last Modified: 2009-07-08
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.