Evidence map›Paper›PMID 27925187›Full record

ArticleImmunology2017

Depletion of CD52-positive cells inhibits the development of central nervous system autoimmune disease, but deletes an immune-tolerance promoting CD8 T-cell population. Implications for secondary autoimmunity of alemtuzumab in multiple sclerosis.

Stephanie von Kutzleben, Gareth Pryce, Gavin Giovannoni, David Baker

Open access · hybridAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed, 2 pooled it
5.7field-weighted citation impact, top 3% 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

25 citing papers in PubMed, 2 syntheses or guidelines pooled it, 54 citations in OpenAlex.

  1. Alemtuzumab and thrombotic thrombocytopenic purpura: Analysis of an international surveillance database and systematic literature review.Transfusion and apheresis science : official journal of the World Apheresis Association : official journal of the European Society for Haemapheresis · 2025
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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

4 authors at 1 institution in 1 country.

Stephanie von KutzlebenNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, London, UK.
Gareth PryceNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, London, UK.
Gavin GiovannoniNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, London, UK.
David BakerNeuroimmunology Unit, Blizard Institute, Barts and the London School of Medicine & Dentistry, Queen Mary University of London, London, UK.
Queen Mary University of London · GB

Funding

Medical Research Council
6 · The paper itself

Abstract

The objective was to determine whether CD52 lymphocyte depletion can act to promote immunological tolerance induction by way of intravenous antigen administration such that it could be used to either improve efficiency of multiple sclerosis (MS) inhibition or inhibit secondary autoimmunities that may occur following alemtuzumab use in MS. Relapsing experimental autoimmune encephalomyelitis was induced in ABH mice and immune cell depletion was therapeutically applied using mouse CD52 or CD4 (in conjunction with CD8 or CD20) depleting monoclonal antibodies. Immunological unresponsiveness was then subsequently induced using intravenous central nervous system antigens and responses were assessed clinically. A dose-response of CD4 monoclonal antibody depletion indicated that the 60-70% functional CD4 T-cell depletion achieved in perceived failed trials in MS was perhaps too low to even stop disease in animals. However, more marked (~75-90%) physical depletion of CD4 T cells by CD4 and CD52 depleting antibodies inhibited relapsing disease. Surprisingly, in contrast to CD4 depletion, CD52 depletion blocked robust immunological unresponsiveness through a mechanism involving CD8 T cells. Although efficacy was related to the level of CD4 T-cell depletion, the observations that CD52 depletion of CD19 B cells was less marked in lymphoid organs than in the blood provides a rationale for the rapid B-cell hyper-repopulation that occurs following alemtuzumab administration in MS. That B cells repopulate in the relative absence of T-cell regulatory mechanisms that promote immune tolerance may account for the secondary B-cell autoimmunities, which occur following alemtuzumab treatment of MS.

Indexed as

AlemtuzumabAnimalsAntibodies, Monoclonal, HumanizedAntigens, CDAntigens, NeoplasmAutoimmunityB-LymphocytesCD4-Positive T-LymphocytesCD52 AntigenCD8-Positive T-LymphocytesCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalFemaleGlycoproteinsHumansImmune ToleranceAlemtuzumabAntibodies, Monoclonal, HumanizedAntigens, CDAntigens, NeoplasmCD52 AntigenCD52 protein, humanGlycoproteinsautoimmunityexperimental autoimmune encephalomyelitis/multiple sclerosisneuroimmunologytolerance/suppression/anergy

Identifiers

PMID27925187
PMCPMC5343359
OpenAlexW2560500860

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.