| dc.contributor.advisor | Reichardt, Holger Prof. Dr. | |
| dc.contributor.author | Witte, Ann-Kathrin | |
| dc.date.accessioned | 2017-11-06T09:42:55Z | |
| dc.date.available | 2017-11-16T23:50:06Z | |
| dc.date.issued | 2017-11-06 | |
| dc.identifier.uri | http://hdl.handle.net/11858/00-1735-0000-0023-3F57-5 | |
| dc.identifier.uri | http://dx.doi.org/10.53846/goediss-6566 | |
| dc.language.iso | deu | de |
| dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | |
| dc.subject.ddc | 610 | de |
| dc.title | Die Rolle des antiapoptotischen Gens Gimap5 für die Pathogenese neuroinflammatorischer Erkrankungen | de |
| dc.type | doctoralThesis | de |
| dc.title.translated | The role of the antiapoptotic gene Gimap5 on the pathogenesis of neuroinflammatory diseases | de |
| dc.contributor.referee | Reichardt, Holger Prof. Dr. | |
| dc.date.examination | 2017-11-09 | |
| dc.description.abstracteng | T-cell lymphopenia is a major risk factor for autoimmunity. A loss-of-function mutation in the Gimap5 gene leads to a reduction in peripheral T-cell numbers in Congenic Lewis rats. Gimap5-deficient Lewis rats developed eosinophilic autoimmune gastroenteritis accompanied by an increase in IgE serum levels. This phenotype was ameliorated by antibiotic treatment, indicating a critical role of the microbial flora in the development of inflammatory bowel disease. Gimap5-deficient Lewis rats showed strongly aggravated experimental autoimmune encephalomyelitis after immunization with guinea pig myelin basic protein. This phenotype, however, persisted after antibiosis, confirming that the enhanced CNS autoimmune response in T-cell lymphopenic Gimap5-deficient Lewis rats was unrelated to the composition of the microbial flora. Rather, it seems that it was caused by the increase in the percentage of activated T cells producing IL-17 and IFN-g, and the skewed T-cell receptor repertoire, both of which were the result of T-cell lymphopenia and not affected by antibiosis. This notion was supported by the observation that adoptive T-cell transfer corrected the T-cell receptor repertoire and improved experimental autoimmune encephalomyelitis. Collectively, the findings confirm a critical albeit differential role of T-cell lymphopenia in the susceptibility to organ-specific autoimmune responses. | de |
| dc.contributor.coReferee | Lühder, Fred PD Dr. | |
| dc.contributor.thirdReferee | Meyer, Thomas Prof. Dr. | |
| dc.subject.eng | experimental autoimmune encephalomyelitis | de |
| dc.subject.eng | eosinophilic bowel disease | de |
| dc.identifier.urn | urn:nbn:de:gbv:7-11858/00-1735-0000-0023-3F57-5-0 | |
| dc.affiliation.institute | Medizinische Fakultät | de |
| dc.subject.gokfull | Medizin (PPN619874732) | de |
| dc.description.embargoed | 2017-11-16 | |
| dc.identifier.ppn | 1002860237 | |