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• W1801413543 abstract "Multiple Sclerosis is most probably an autoimmune inflammatory disease of the central nervous system. Demyelination of neurons and axonal loss occur in temporal and spatial resolution in multiple areas of the brain and spinal cord. This impairment manifests in neurological symptoms. The course of disease varies between individuals and the causing mechanisms still remain elusive. Environmental factors as well as genetic predispositions are widely discussed.Recent studies stressed the prominent role of CD8+ T lymphocytes in the autoimmune pathomechanism. They notably exceed the amount of CD4+ T cells in acute lesions yet target cells and activating antigens remain elusive. A genetic linkage between the human leukocyte antigen gene locus and disease susceptibility was observed. Carrying the HLA A*0301 allele or the HLA A*0201 allele correlates with a risk factor or protective effect for Multiple Sclerosis susceptibility, respectively. Thus during this thesis two main questions were followed:1.Which CD8+ T lymphocytes participate in the autoimmune attack on central nervous system tissue and what are their receptors for antigen recognition?2.How does the expression of HLA-A2 molecules lead to a decreased disease susceptibility?In the first part, the T cell receptor molecules of potentially disease-related single CD8+ T cells from frozen patient tissue samples were characterized. T lymphocytes were considered disease-related when they either belonged to a clonally expanded T cell population or expressed an activation marker on their cell surface. In a clone-specific approach, the T cell receptor beta chains of pre-analyzed, clonally expanded T cell populations were investigated. Further an unbiased approach independent of pre-analyses was established.In the second part, antigen recognition of the probably disease-related T cell receptor 2D1 was investigated. This receptor was isolated from a Multiple Sclerosis patient and was known to be activated by a myelin-derived peptide presented on HLA-A3 molecules. In an animal model double-transgenic mice expressing HLA-A3 and the 2D1 T cell receptor developed a Multiple Sclerosis-like disease after immunization with the known peptide. Surprisingly not a single triple-transgenic mouse expressing HLA-A3, the T cell receptor 2D1 and HLA-A2 showed symptoms after immunization. In these mice 2D1 T lymphocytes were shown to be depleted in the thymus.To characterize HLA-A2-bound peptides which mediate this protective effect a novel technology for unbiased identification of antigenic peptides recognized by human leukocyte antigen class I-restricted T lymphocytes was employed. 28 peptides presented on HLA-A2 molecules were found to be recognized by the T cell receptor 2D1. Those peptides displayed very closely related sequences. Eight possible parent proteins existing in mouse, therefrom even four equally expressed in humans were identified. Finally those putative parent proteins were further characterized and first investigations of antigen processing in different antigen presenting cell lines were performed." @default.
• W1801413543 created "2016-06-24" @default.
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• W1801413543 date "2014-08-22" @default.
• W1801413543 modified "2023-09-27" @default.
• W1801413543 title "Characterization of disease-related CD8+ T cells and their antigens from patients with Multiple Sclerosis" @default.
• W1801413543 hasPublicationYear "2014" @default.
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