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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
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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.
Find related publications in this database (using NLM MeSH Indexing)
Animals -
Antibodies - blood
Antibody Formation - immunology
Cell Count -
Disease Susceptibility - etiology
Encephalomyelitis, Autoimmune, Experimental - etiology
Endothelial Cells - metabolism
Lymph Nodes - metabolism
Lymphocyte Activation - immunology
Macrophages - cytology
Membrane Proteins - deficiency
Mice -
Mice, Inbred C57BL -
Mice, Mutant Strains -
Microglia - cytology
Myelin-Associated Glycoprotein - immunology
Peptide Fragments - immunology
Spinal Cord - pathology
Spleen - metabolism
T-Lymphocytes - cytology
Vaccination -

Find related publications in this database (Keywords)
EAE
CNS
inflammation
T cells
dysferlin
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