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Reinhard Hohlfeld

Researcher at Ludwig Maximilian University of Munich

Publications -  171
Citations -  18019

Reinhard Hohlfeld is an academic researcher from Ludwig Maximilian University of Munich. The author has contributed to research in topics: Multiple sclerosis & Antigen. The author has an hindex of 64, co-authored 170 publications receiving 16438 citations. Previous affiliations of Reinhard Hohlfeld include Max Planck Society & University of Düsseldorf.

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A Placebo-Controlled Trial of Oral Fingolimod in Relapsing Multiple Sclerosis

TL;DR: Both doses of oral fingolimod improved the relapse rate, the risk of disability progression, and end points on MRI and were superior to placebo with regard to MRI-related measures.
Book

Polymyositis and Dermatomyositis

TL;DR: Early initiation of therapy is essential, since both polymyositis and dermatomyositis respond to immunotherapeutic agents and new immunomodulatory agents currently being tested in controlled trials may prove promising for difficult cases.
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Clonal Expansions of Cd8+ T Cells Dominate the T Cell Infiltrate in Active Multiple Sclerosis Lesions as Shown by Micromanipulation and Single Cell Polymerase Chain Reaction

TL;DR: Clonal composition and T cell receptor (TCR) repertoire of CD4+ and CD8+ T cells infiltrating actively demyelinating multiple sclerosis (MS) lesions were determined with unprecedented resolution at the level of single cells.
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Gut microbiota from multiple sclerosis patients enables spontaneous autoimmune encephalomyelitis in mice.

TL;DR: Evidence is provided that MS-derived microbiota contain factors that precipitate an MS-like autoimmune disease in a transgenic mouse model, and the results offer functional evidence that human microbiome components contribute to CNS-specific autoimmunity.
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MicroRNA profiling of multiple sclerosis lesions identifies modulators of the regulatory protein CD47

TL;DR: It is suggested that microRNA dysregulated in multiple sclerosis lesions reduce CD47 in brain resident cells, releasing macrophages from inhibitory control, thereby promoting phagocytosis of myelin and have broad implications for microRNA-regulated macrophage activation in inflammatory diseases.