ReviewHuman vaccines & immunotherapeutics2018
Immunotherapy of Guillain-Barré syndrome.
Review in Human vaccines & immunotherapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 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
38 citing papers in PubMed, 56 citations in OpenAlex.
- Efgartigimod for Guillain-Barré syndrome: a retrospective analysis of efficacy and safety.Therapeutic advances in neurological disorders · 2026Article
- A Review of Cutaneous Viral Infections and Their Potential Role in Neurologic Diseases.Journal of clinical medicine · 2025Review
- Article
- Peripheral nerve-targeting and pain-promoting transcriptomic signatures in early Guillain-Barré syndrome.bioRxiv : the preprint server for biology · 2025Article
- Article
- Small Nuclear Ribonucleoprotein Autoantibody Associated With Blood-Nerve Barrier Breakdown in Guillain-Barré Syndrome.Neurology(R) neuroimmunology & neuroinflammation · 2025Article
- Using Olink Proteomics to Identify Inflammatory Biomarkers in the Cerebrospinal Fluid in Guillain-Barré Syndrome.Journal of inflammation research · 2025Article
- Evolving understanding of Guillain-Barré syndrome pathophysiology and the central role of the classical complement pathway in axonal injury.Frontiers in neurology · 2025Article
- Article
- Animal models of immune-mediated demyelinating polyneuropathies.Autoimmunity · 2024Review
- Causal role of the pyrimidine deoxyribonucleoside degradation superpathway mediation in Guillain-Barré Syndrome via the HVEM on CD4 + and CD8 + T cells.Scientific reports · 2024Article
- Rapid Improvement in Guillain-Barré Syndrome With Demyelinating and Secondary Axonal Involvement: A Case Report.Cureus · 2024Article
- Lower Limb Paralysis Associated with Chikungunya in Kinshasa, the Democratic Republic of the Congo: Survey Report.Pathogens (Basel, Switzerland) · 2024Article
- Plasma exchange (PE) versus intravenous immunoglobulin (IVIG) for the treatment of Guillain-Barré syndrome (GBS) in patients with severe symptoms: A systematic review and meta-analysis.eNeurologicalSci · 2023Review
- Article
- A diagnostic support system based on pain drawings: binary and k-disease classification of EDS, GBS, FSHD, PROMM, and a control group with Pain2D.Orphanet journal of rare diseases · 2023Article
- Neuron-Schwann cell interactions in peripheral nervous system homeostasis, disease, and preclinical treatment.Frontiers in cellular neuroscience · 2023Review
- Regulatory Mechanism of M1/M2 Macrophage Polarization in the Development of Autoimmune Diseases.Mediators of inflammation · 2023Review
- Diagnostic Pitfalls in Guillain-Barré Syndrome: Case Report and Literature Review.Children (Basel, Switzerland) · 2022Review
- Intravenous immunoglobulin prevents peripheral liver transduction of intrathecally delivered AAV vectors.Molecular therapy. Methods & clinical development · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Guillain-Barré syndrome (GBS), the most common cause of acute neuromuscular weakness and paralysis worldwide, encompasses a group of acute immune-mediated disorders restricted to peripheral nerves and roots. Immune-mediated attack of peripheral nervous system myelin, axons or both is presumed to be triggered by molecular mimicry, with both cell- and humoral-dependent mechanisms implicated in disease pathogenesis. Good circumstantial evidence exists for a pathogenic role for molecular mimicry in GBS pathogenesis, especially with its axonal forms, providing insights that could guide future immunotherapy. Intravenous immunoglobulin (IVIg) and plasma exchange (PE) are the most commonly prescribed immunotherapies for GBS with variable efficacy dependent on GBS subtype, severity at initial presentation and other clinical and electrophysiologic prognostic factors. The mechanisms of action of IVIg and PE are not known definitely. Despite recent significant advances in molecular biology that provide insights into GBS pathogenesis, no advances in therapeutics or significant improvements in patient outcomes have occurred over the past three decades. We summarize the clinical aspects of GBS, its current pathogenesis and immunotherapy, and highlight the potential of leukocyte trafficking inhibitors as novel disease-specific immunotherapeutic drugs.
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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.