Evidence map›Paper›PMID 22027448›Full record

ArticleJournal of neuroinflammation2011

Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders.

Klaus Lehmann-Horn, Eva Schleich, Deetje Hertzenberg, Alexander Hapfelmeier, Tania Kümpfel, Nikolas von Bubnoff, Reinhard Hohlfeld, Achim Berthele, Bernhard Hemmer, Martin S Weber

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
2.6field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

49 citing papers in PubMed, 81 citations in OpenAlex.

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  15. A Milestone in Multiple Sclerosis Therapy: Monoclonal Antibodies Against CD20-Yet Progress Continues.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
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  20. B cells reappear less mature and more activated after their anti-CD20-mediated depletion in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2020
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Klaus Lehmann-HornDepartment of Neurology, Technische Universität München, Munich, Germany.
Eva Schleich
Deetje Hertzenberg
Alexander Hapfelmeier
Tania Kümpfel
Nikolas von Bubnoff
Reinhard Hohlfeld
Achim Berthele
Bernhard Hemmer
Martin S Weber
Technical University of Munich · DELudwig-Maximilians-Universität München · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundClinical trials evaluating anti-CD20-mediated B-cell depletion in multiple sclerosis (MS) and neuromyelitis optica (NMO) generated encouraging results. Our recent studies in the MS model experimental autoimmune encephalomyelitis (EAE) attributed clinical benefit to extinction of activated B-cells, but cautioned that depletion of naïve B-cells may be undesirable. We elucidated the regulatory role of un-activated B-cells in EAE and investigated whether anti-CD20 may collaterally diminish regulatory B-cell properties in treatment of neuroimmunological disorders.

methodsMyelin oligodendrocyte glycoprotein (MOG) peptide-immunized C57Bl/6 mice were depleted of B-cells. Functional consequences for regulatory T-cells (Treg) and cytokine production of CD11b+ antigen presenting cells (APC) were assessed. Peripheral blood mononuclear cells from 22 patients receiving anti-CD20 and 23 untreated neuroimmunological patients were evaluated for frequencies of B-cells, T-cells and monocytes; monocytic reactivity was determined by TNF-production and expression of signalling lymphocytic activation molecule (SLAM).

resultsWe observed that EAE-exacerbation upon depletion of un-activated B-cells closely correlated with an enhanced production of pro-inflammatory TNF by CD11b+ APC. Paralleling this pre-clinical finding, anti-CD20 treatment of human neuroimmunological disorders increased the relative frequency of monocytes and accentuated pro-inflammatory monocyte function; when reactivated ex vivo, a higher frequency of monocytes from B-cell depleted patients produced TNF and expressed the activation marker SLAM.

conclusionsThese data suggest that in neuroimmunological disorders, pro-inflammatory APC activity is controlled by a subset of B-cells which is eliminated concomitantly upon anti-CD20 treatment. While this observation does not conflict with the general concept of B-cell depletion in human autoimmunity, it implies that its safety and effectiveness may further advance by selectively targeting pathogenic B-cell function.

Indexed as

AnimalsAntigens, CDAntigens, CD20Autoimmune DiseasesB-LymphocytesCD11b AntigenEncephalomyelitis, Autoimmune, ExperimentalHumansMiceMice, Inbred C57BLMonocytesMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsNeuroimmunomodulationReceptors, Cell SurfaceSignaling Lymphocytic Activation Molecule Family Member 1Antigens, CDAntigens, CD20CD11b AntigenMOG protein, humanMog protein, mouseMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsReceptors, Cell SurfaceSignaling Lymphocytic Activation Molecule Family Member 1Tumor Necrosis Factor-alpha

Identifiers

PMID22027448
PMCPMC3214191
OpenAlexW2130318414

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.