Literature DB >> 8982117

Soluble complement receptor 1 (sCR1) protects against experimental autoimmune myasthenia gravis.

S J Piddlesden1, S Jiang, J L Levin, A Vincent, B P Morgan.   

Abstract

The loss of muscle function seen in myasthenia gravis and in the animal model of the disease, experimental autoimmune myasthenia gravis (EAMG) is in part due to the activation of complement by anti-acetylcholine receptor (AChR) antibodies at the motor end-plate. In this study we describe the effects of a soluble recombinant form of human complement receptor 1 (sCR1) on the development of clinical disease and receptor loss in EAMG induced passively by administration of anti-AChR antibodies. Daily intraperitoneal injection of sCR1 significantly reduced the weight loss and severity of clinical symptoms seen and allowed treated animals to recover normal muscle function. These data suggest that sCR1 could provide a useful additional therapeutic agent in myasthenia.

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Year:  1996        PMID: 8982117     DOI: 10.1016/s0165-5728(96)00144-0

Source DB:  PubMed          Journal:  J Neuroimmunol        ISSN: 0165-5728            Impact factor:   3.478


  37 in total

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9.  Extraocular muscle susceptibility to myasthenia gravis: unique immunological environment?

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10.  A functional SNP in the regulatory region of the decay-accelerating factor gene associates with extraocular muscle pareses in myasthenia gravis.

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