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H.-Christian von Büdingen

Researcher at University of California, San Francisco

Publications -  28
Citations -  1804

H.-Christian von Büdingen is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Multiple sclerosis & Medicine. The author has an hindex of 15, co-authored 21 publications receiving 1300 citations. Previous affiliations of H.-Christian von Büdingen include University of Zurich & Technische Universität München.

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Update on the Autoimmune Pathology of Multiple Sclerosis: B-Cells as Disease-Drivers and Therapeutic Targets

TL;DR: The goal of this review is to summarize how B-cells may contribute to MS pathogenesis and thereby provide a basis for understanding why B-cell depletion is so effective in the treatment of this disease.
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Rituximab Efficiently Depletes Increased CD20-Expressing T Cells in Multiple Sclerosis Patients

TL;DR: It is shown that in MS patients, increased levels of CD3+CD20dim T cells are effectively depleted by RTX, and depletion of CD20-expressing T cells may also contribute to the therapeutic effect of RTX and other mAbs targeting CD20.
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B cell exchange across the blood-brain barrier in multiple sclerosis

TL;DR: In this paper, the authors applied deep repertoire sequencing of IgG heavy chain variable region genes (IgG-VH) in paired cerebrospinal fluid and PB samples from patients with MS and other neurological diseases to identify related B cells that are common to both compartments.
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Immunoglobulin class-switched B cells form an active immune axis between CNS and periphery in multiple sclerosis.

TL;DR: Pinpointing Ig class-switched B cells as key component of the immune axis thought to contribute to ongoing MS disease activity strengthens the rationale of current B cell–targeting therapeutic strategies and may lead to more targeted approaches.
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Naive antibody gene-segment frequencies are heritable and unaltered by chronic lymphocyte ablation

TL;DR: Using high-throughput sequence analysis of monozygotic twins, it is shown that variation in naive VH and DH segment use is strongly determined by an individual's germ-line genetic background and may provide a unique mechanism for stratifying individual risk profiles in specific diseases.