ArticleFrontiers in immunology2023
Immune reconstitution following alemtuzumab therapy is characterized by exhausted T cells, increased regulatory control of proinflammatory T cells and reduced B cell control.
Article in Frontiers in immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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.
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.
Who cites it
12 citing papers in PubMed.
- Confined B-Cell Reconstruction and High T-Cell Clonality Define Clinical Response to Cladribine Treatment.Annals of neurology · 2026Article
- Review
- T cell-mediated immunodysregulation in multiple sclerosis: from pathogenic subsets to therapeutic advances.Frontiers in immunology · 2026Review
- A stepwise institutional approach to refractory autoimmune cytopenia after allogeneic stem cell transplantation in children: a retrospective case series.Frontiers in immunology · 2026Article
- Redefining multiple sclerosis therapy through microbial immunomodulation and epigenetic control.Journal of translational autoimmunity · 2025Review
- Immunological Monitoring During Anti-CD20 Therapies to Predict Infection Risk and Treatment Response in Multiple Sclerosis Patients.Diseases (Basel, Switzerland) · 2025Article
- Mechanistic Insights into Drug-Induced Guillain-Barré Syndrome: A Large-Cohort Analysis of the FAERS Database.Pharmaceuticals (Basel, Switzerland) · 2025Article
- Modulator of VRAC Current 1 Is a Potential Target Antigen in Multiple Sclerosis.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Understanding Pediatric Kidney Transplant Rejection: Its Pathophysiology, Biomarkers, and Management Strategies.Current medicinal chemistry · 2025Review
- B-cell-driven relapse and anti-CD20 rescue therapy after Alemtuzumab in RRMS: case report and literature review.Frontiers in immunology · 2025Review
- New autoimmune disorder development after immune reconstitution therapy for multiple sclerosis.Scientific reports · 2024Article
- The immunological bases of alemtuzumab as induction-therapy in pediatric-onset multiple sclerosis.Frontiers in immunology · 2024Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alemtuzumab is a monoclonal antibody targeting CD52 on the surface of immune cells, approved for the treatment of active relapsing-remitting multiple sclerosis (RRMS). The purpose of this study was to analyze the repopulation of peripheral lymphocytes following alemtuzumab-induced lymphocyte depletion and investigate associations with disease activity and development of secondary autoimmunity. For this, blood samples were collected two years after initiation of alemtuzumab treatment and lymphocytes were subjected to a comprehensive flow cytometry analysis. Included in the study were 40 patients treated with alemtuzumab and 40 treatment-naïve patients with RRMS. Disease activity and development of secondary autoimmune disease was evaluated after three years of treatment. Our study confirms that alemtuzumab treatment profoundly alters the circulating lymphocyte phenotype and describes a reconstituted immune system characterized by T cell activation/exhaustion, an increased regulatory control of IL-17 producing effector T cells and CD20
Indexed as
Identifiers
What OpenQuestion holds
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.