kim Posted September 10, 2009 Report Share Posted September 10, 2009 Buster or EAMom, is this an area that you are familiar with at all? When I said that I was dying to know what was different about the mouse in the Cunningham study, I was almost expecting to see this type of mouse. Also, I remember Buster making a remark about the "chain" possibly being abnormal in the first place, or something like that in a post somewhere. This is an area of extreme interest to me, altho horribly frustrating! bolding mine http://www.ncbi.nlm.nih.gov/pubmed/1856786...ogdbfrom=pubmed Our work has focused on axonal and glial components of the motor nerve terminal as a model site of injury, and through combined active and passive immunization paradigms in glycosyltransferase knockout mice we have developed murine neuropathy phenotypes mediated by anti-ganglioside antibodies. Several determinants influence disease expression including the level of immunological tolerance to microbial glycans that mimic self gangliosides, the degree of complement activation, and the ganglioside density in target tissue. Such studies provide us with clear information on an antibody-mediated pathogenesis model for GBS and should lead to rational therapeutic testing of agents that are potentially suitable for use in man. Link to comment Share on other sites More sharing options...
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