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Hochmeister, S; Bittner, RE; Höger, H; Lassmann, H; Bradl, M.
The susceptibility to experimental autoimmune encephalomyelitis is not related to dysferlin-deficiency.
Autoimmunity. 2009; 42(3): 235-241.
Doi: 10.1080/08916930802716542
Web of Science
PubMed
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- Führende Autor*innen der Med Uni Graz
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Hochmeister Sonja
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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.
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Animals -
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Antibodies - blood
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Antibody Formation - immunology
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Cell Count -
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Disease Susceptibility - etiology
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Encephalomyelitis, Autoimmune, Experimental - etiology
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Endothelial Cells - metabolism
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Lymph Nodes - metabolism
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Lymphocyte Activation - immunology
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Macrophages - cytology
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Membrane Proteins - deficiency
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Mice -
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Mice, Inbred C57BL -
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Mice, Mutant Strains -
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Microglia - cytology
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Myelin-Associated Glycoprotein - immunology
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Peptide Fragments - immunology
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Spinal Cord - pathology
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Spleen - metabolism
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T-Lymphocytes - cytology
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Vaccination -
- Find related publications in this database (Keywords)
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EAE
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CNS
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inflammation
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T cells
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dysferlin