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Ludger Klein

Researcher at Ludwig Maximilian University of Munich

Publications -  65
Citations -  16650

Ludger Klein is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: T cell & Central tolerance. The author has an hindex of 38, co-authored 64 publications receiving 14903 citations. Previous affiliations of Ludger Klein include German Cancer Research Center & Research Institute of Molecular Pathology.

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Guidelines for the use and interpretation of assays for monitoring autophagy

Daniel J. Klionsky, +1287 more
- 01 Apr 2012 - 
TL;DR: These guidelines are presented for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes.
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Projection of an Immunological Self Shadow Within the Thymus by the Aire Protein

TL;DR: Aire-deficient thymic medullary epithelial cells showed a specific reduction in ectopic transcription of genes encoding peripheral antigens, highlighting the importance of thymically imposed “central” tolerance in controlling autoimmunity.
Journal ArticleDOI

Positive and negative selection of the T cell repertoire: what thymocytes see (and don't see).

TL;DR: It is discussed how the particular composition of the peptide–MHC ligandomes that are presented by specific APC subsets not only shapes the T cell repertoire in the thymus but may also indelibly imprint the behaviour of mature T cells in the periphery.
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Promiscuous gene expression in medullary thymic epithelial cells mirrors the peripheral self.

TL;DR: It is found that this promiscuous gene expression was a cell-autonomous property of medullary epithelial cells and was maintained during the entire period of thymic T cell output, which may facilitate tolerance induction to self-antigens that would otherwise be temporally or spatially secluded from the immune system.
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Origin of regulatory T cells with known specificity for antigen

TL;DR: The immunoglobulin κ–controlled expression of an agonist in different cell types correlated with the phenotype of the generated TR cells, and it was found that aberrant expression on thymic stroma yielded predominantly CD4+CD25+TR cells, which—under physiological conditions—may be induced by ectopically expressed organ-specific antigens and thus prevent organ- specific autoimmunity.