Evidence map›Paper›PMID 33324905›Full record

Trial reportNeurological research and practice2019

Signatures of immune reprogramming in anti-CD52 therapy of MS: markers for risk stratification and treatment response.

Laura Bierhansl, Tobias Ruck, Steffen Pfeuffer, Catharina C Gross, Heinz Wiendl, Sven G Meuth

Registry-linked trialOpen access · diamondAbstract readClinical Trial
In one paragraph

Trial report in Neurological research and practice, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT04082260 (Signatures of Immune Reprogramming in Anti-CD52 Therapy of MS), which is not on this map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.6field-weighted citation impact, top 30% 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.

NCT04082260 unknown statusnot on this map

Signatures of Immune Reprogramming in Anti-CD52 Therapy of MS: Markers for Risk Stratification and Treatment Response

TypeobservationalSponsorUniversity Hospital MuensterRan2017 to 2022Enrolled150ConditionsMultiple SclerosisArmsAlemtuzumab Injection [Lemtrada]
3 · Its place in the literature

Who cites it

5 citing papers in PubMed, 6 citations in OpenAlex.

  1. Modulator of VRAC Current 1 Is a Potential Target Antigen in Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2025
    Article
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  3. Review
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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

6 authors at 1 institution in 1 country.

Laura BierhanslDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.ORCID 0000-0002-6752-690X
Tobias RuckDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Steffen PfeufferDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Catharina C GrossDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Heinz WiendlDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
Sven G MeuthDepartment of Neurology with Institute of Translational Neurology, University Hospital Muenster, Albert-Schweitzer-Campus 1, 48149 Muenster, Germany.
University Hospital Münster · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMultiple sclerosis is one of the most prevalent neurological diseases in young adults affecting over 2 million people worldwide. Alemtuzumab is a highly effective therapy in relapsing remitting MS. Alemtuzumab is a monoclonal CD52 antibody that proved its efficacy against an active comparator (interferon [IFN]-β1a) in a phase II trial and two phase III trials regarding clinical and MRI outcomes. Nevertheless, the exact mode of action is still unknown. Alemtuzumab is commonly associated with secondary autoimmune disorders significantly affecting the risk-benefit ratio. Therefore, new biomarkers predicting treatment response and adverse events are urgently needed. This study aims to further elucidate the mechanism of action of the neuroprotective potential of alemtuzumab in relapsing-remitting multiple sclerosis (RRMS). METHODS/

designThis is a 3-year multicentre, explorative study including overall 150 patients comprising three different groups: (i) de novo patients prior and after alemtuzumab treatment initiation, (ii) patients under alemtuzumab treatment and (iii) patients requiring more than two alemtuzumab infusions. Peripheral blood and serum samples will be collected semi-annually for several in vitro/ex vivo assays to detect and characterize immune cells including their functional activity. Furthermore, data of MRI scans and disease-related impairment (using EDSS and MSFC), as well as the number and time of relapses, will be assessed. The clinical study is registered at clinicaltrials.gov (NCT04082260). PERSPECTIVE: Our study will provide deep insights into the underlying immunological changes in a longitudinal analysis of alemtuzumab treated RRMS patients. By combining clinical, radiological and functional immune-phenotype data, we will be able to identify biomarkers and/or immune signatures predicting treatment response and adverse events. Thereby, the understanding of the mechanisms of action of alemtuzumab will improve its efficacy and safety for present and future patients.

Indexed as

AlemtuzumabBiomarker, mechanism of action, secondary autoimmune diseaseCD52Disease-modifying therapy, risk stratificationRelapse-remitting multiple sclerosis

Identifiers

PMID33324905
PMCPMC7650051
OpenAlexW2995608790

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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.