Myocytes respond in vivo to an antibody reactive with the acetylcholine receptor by upregulating interleukin-15: an interferon-gamma activator with the potential to influence the severity and course of experimental myasthenia gravis.

Authors: Stegall, T  Krolick, KA 
Citation: Stegall T and Krolick KA, J Neuroimmunol. 2001 Oct 1;119(2):377-86.
Pubmed: (View Article at PubMed) PMID:11585642

The monoclonal antibody, mAb35, which binds the main immunogenic region of the post-junctional muscle receptor for acetylcholine (AChR), results in contractile dysfunction and symptoms of experimental myasthenia gravis (EAMG). As described below, exposure to mAb35 also results in the production by muscle of increased levels of the interferon-gamma (IFN-gamma)-activating cytokine, interleukin-15. This effect is accompanied by the increased trafficking of leukocytes through muscle, some that produce IFN-gamma. These observations may be relevant to the induction of disease symptoms since numerous reports from other investigators indicate that IFN-gamma may play a pivotal role in this disease process.

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CRRD Object Information
CRRD ID: 1626617
Created: 2007-08-13
Species: All species
Last Modified: 2007-08-13
Status: ACTIVE



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