Evidence map›Paper›PMID 32655545›Full record

ReviewFrontiers in immunology2020

Immunological Bases of Paraneoplastic Cerebellar Degeneration and Therapeutic Implications.

Lidia Yshii, Chloé Bost, Roland Liblau

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in immunology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
3.1field-weighted citation impact, top 6% 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

36 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Narcolepsy is (not) an autoimmune disease.Nature reviews. Neurology · 2026
    Review
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  14. Blood-Brain Barrier Disruption in Neuroimmunological Disease.International journal of molecular sciences · 2024
    Review
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  16. Article
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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

3 authors at 3 institutions in 1 country.

Lidia YshiiINSERM U1043, CNRS UMR 5282, Université Toulouse III, Center for Pathophysiology Toulouse Purpan, Toulouse, France.
Chloé BostINSERM U1043, CNRS UMR 5282, Université Toulouse III, Center for Pathophysiology Toulouse Purpan, Toulouse, France.
Roland LiblauINSERM U1043, CNRS UMR 5282, Université Toulouse III, Center for Pathophysiology Toulouse Purpan, Toulouse, France.
Centre de Physiopathologie de Toulouse-Purpan · FRCentre National de la Recherche Scientifique · FRUniversité Toulouse III - Paul Sabatier · FR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Paraneoplastic cerebellar degeneration (PCD) is a rare immune-mediated disease that develops mostly in the setting of neoplasia and offers a unique prospect to explore the interplay between tumor immunity and autoimmunity. In PCD, the deleterious adaptive immune response targets self-antigens aberrantly expressed by tumor cells, mostly gynecological cancers, and physiologically expressed by the Purkinje neurons of the cerebellum. Highly specific anti-neuronal antibodies in the serum and cerebrospinal fluid represent key diagnostic biomarkers of PCD. Some anti-neuronal antibodies such as anti-Yo autoantibodies (recognizing the CDR2/CDR2L proteins) are only associated with PCD. Other anti-neuronal antibodies, such as anti-Hu, anti-Ri, and anti-Ma2, are detected in patients with PCD or other types of paraneoplastic neurological manifestations. Importantly, these autoantibodies cannot transfer disease and evidence for a pathogenic role of autoreactive T cells is accumulating. However, the precise mechanisms responsible for disruption of self-tolerance to neuronal self-antigens in the cancer setting and the pathways involved in pathogenesis within the cerebellum remain to be fully deciphered. Although the occurrence of PCD is rare, the risk for such severe complication may increase with wider use of cancer immunotherapy, notably immune checkpoint blockade. Here, we review recent literature pertaining to the pathophysiology of PCD and propose an immune scheme underlying this disabling disease. Additionally, based on observations from patients' samples and on the pre-clinical model we recently developed, we discuss potential therapeutic strategies that could blunt this cerebellum-specific autoimmune disease.

Indexed as

AutoimmunityAnimalsAntigens, NeoplasmAutoantibodiesAutoantigensCerebellumHumansImmunotherapyNeoplasmsNerve Tissue ProteinsParaneoplastic Cerebellar DegenerationPurkinje CellsRisk FactorsT-LymphocytesAntigens, NeoplasmAutoantibodiesAutoantigensCDR2L antigen, humanCDR2 protein, humanNerve Tissue Proteinsanimal modelanti-neuronal antibodiesautoimmunityimmunotherapyparaneoplastic cerebellar degenerationT cell

Identifiers

PMID32655545
PMCPMC7326021
OpenAlexW3033213169

What OpenQuestion holds

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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.