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Abstract
Recent observations suggested that dysferlin might play a role in the development of autoimmune central nervous system (CNS) inflammation. To address this issue, we studied the induction and effector phase of experimental autoimmune encephalomyelitis in C57BL/10 mice producing intact or functionally deficient dysferlin. We found that both types of mice showed identical T-cell and antibody responses against the immunogen, and developed CNS inflammation with identical clinical courses, frequencies, lesion distributions, sizes and compositions. These findings suggest that the presence or absence of dysferlin does not have any consequences for the triggering or effector phase of autoimmune CNS inflammation.
Acknowledgements
We thank Marianne Leisser, Ulli Köck, and Angela Kury for excellent technical assistance. Our work was supported by the Fonds zur Förderung der wissenschaftlichen Forschung (FWF project P16047-B02 to MB), by the European Commission (grant QLG3-CT-2002-00612 to HL), and by the Neuromuscular Research Department.
Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.