| dc.contributor.advisor | Stadelmann-Nessler, Christine Prof. Dr. | |
| dc.contributor.author | Saß, Benjamin | |
| dc.date.accessioned | 2018-06-01T08:56:52Z | |
| dc.date.available | 2018-06-14T22:50:07Z | |
| dc.date.issued | 2018-06-01 | |
| dc.identifier.uri | http://hdl.handle.net/11858/00-1735-0000-002E-E40C-B | |
| dc.identifier.uri | http://dx.doi.org/10.53846/goediss-6877 | |
| dc.language.iso | deu | de |
| dc.rights.uri | http://creativecommons.org/licenses/by-nc-nd/4.0/ | |
| dc.subject.ddc | 610 | de |
| dc.title | Der Einfluss von Interleukin-3 auf die Läsionslast der experimentellen autoimmunen Enzephalomyelitis | de |
| dc.type | doctoralThesis | de |
| dc.title.translated | The influence of interleukin-3 on the lesion load of EAE | de |
| dc.contributor.referee | Stadelmann-Nessler, Christine Prof. Dr. | |
| dc.date.examination | 2018-06-07 | |
| dc.description.abstracteng | Multiple sclerosis is an inflammatory disease of the central nervous system. Despite decades of research its etiology remains unclear. Keeping in mind that experimental autoimmune encephalomyelitis is an artificially induced disease in animals and differs in many ways from MS, it can nevertheless serve as an useful model for understanding aspects of the pathology of the disease.
Recently, GM-CSF has gained attention in the context of EAE induction and MS pathology. The hematopoietic and proinflammatory Interleukin-3 belongs to the same cytokine family and shares a receptor subunit with GM-CSF. However, its role in EAE and MS has not been focused on so far. Consequently, goal of this study was to investigate the influence of IL-3 on EAE-induction.
We induced EAE in C57BL/6 (H-2b)-mice with MOG (35-55) peptide. In a first trial, mice received IL-3 intraperitoneal from day 5 after EAE induction compared to a control group. Three other trials targeted on the influence of anti-IL-3 antibody application during EAE induction. In the latter trials, control groups received IgG during EAE induction. The clinical course was detected using the EAE score. The mice were sacrificed and prepared for histologically staining. We used LFB/PAS staining to measure the lesion load. CD3 immunohistochemical staining was performed to measure t-cell infiltration.
We found a significant increase of the lesion load and a not significantly higher number of t-cells after the application of IL-3. Furthermore, IL-3 treated mice were clinically more affected. On the other hand, anti-IL-3 antibody treated mice were neither clinically nor histologically healthier than IgG-treated controls.
We conclude that IL-3 is able to boost an inflammatory disease like EAE and therefore might play an important role in EAE-pathology and MS. However, we could not prove that IL-3 is crucial for EAE induction and thus a promising therapeutic target, which might be partially due to the study design. Further trials should include a completely untreated control group and additionally investigate a combined treatment with anti-IL-3 and anti-GM-CSF antibodies. | de |
| dc.contributor.coReferee | Flügel, Alexander Prof. Dr. | |
| dc.subject.ger | Experimentelle autoimmune Enzephalomyelitis | de |
| dc.subject.ger | Multiple Sklerose | de |
| dc.subject.ger | Interlukin-3 | de |
| dc.subject.ger | IL-3 | de |
| dc.subject.ger | Läsionslast | de |
| dc.subject.eng | multiple sclerosis | de |
| dc.subject.eng | experimental autoimmune encephalomyelitis | de |
| dc.subject.eng | interleukin-3 | de |
| dc.identifier.urn | urn:nbn:de:gbv:7-11858/00-1735-0000-002E-E40C-B-0 | |
| dc.affiliation.institute | Medizinische Fakultät | de |
| dc.subject.gokfull | Medizin (PPN619874732) | de |
| dc.description.embargoed | 2018-06-14 | |
| dc.identifier.ppn | 1023648806 | |