Evidence map›Paper›PMID 35689766›Full record

ArticleMolecular neurobiology2022

T cells from MS Patients with High Disease Severity Are Insensitive to an Immune-Suppressive Effect of Sulfatide.

Mio Hamatani, Hirofumi Ochi, Kimitoshi Kimura, Shinji Ashida, Yuichiro Hashi, Yoichiro Okada, Chihiro Fujii, Kazuyuki Kawamura, Toshiki Mizuno, Hideki Ueno and 2 more

Abstract read
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In one paragraph

Article in Molecular neurobiology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
0.3field-weighted citation impact, top 46% 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

2 citing papers in PubMed, 4 citations in OpenAlex.

  1. Review
  2. Article
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

12 authors at 5 institutions in 1 country.

Mio HamataniInstitute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan.
Hirofumi OchiDepartment of Geriatric Medicine and Neurology, Ehime University Graduate School of Medicine, Toon, Japan.
Kimitoshi KimuraDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Shinji AshidaDepartment of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Yuichiro HashiDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Yoichiro OkadaDepartment of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
Chihiro FujiiDepartment of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Kazuyuki KawamuraDepartment of Neurology, National Hospital Organization Minami Kyoto Hospital, Kyoto, Japan.
Toshiki MizunoDepartment of Neurology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Hideki UenoInstitute for the Advanced Study of Human Biology, Kyoto University, Kyoto, Japan.
Ryosuke TakahashiDepartment of Geriatric Medicine and Neurology, Ehime University Graduate School of Medicine, Toon, Japan.
Takayuki KondoDepartment of Neurology, Kansai Medical University Medical Center, Moriguchi, Japan. takakon78@hotmail.com.ORCID http://orcid.org/0000-0001-7048-9401
Kansai Medical University · JPKyoto Prefectural University of Medicine · JPKyoto University · JPEhime University · JPKyoto Medical Center · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Multiple sclerosis (MS) is a chronic inflammatory demyelinating disease of the central nervous system (CNS). Its early phase is characterized by a relapse-remitting disease course, followed by disability progression in the later stage. While chronic inflammation accompanied with degeneration is well-established as the key pathological feature, the pathogenesis of MS, particularly progressive MS, remains elusive. Sulfatide is a major glycolipid component of myelin, and previous studies in experimental autoimmune encephalomyelitis mouse models have demonstrated it to have immune-protective functions. Notably, sulfatide concentration is increased in the serum and cerebrospinal fluid of patients with MS, particularly those in a progressive disease course. Here, we show that the myelin-glycolipid sulfatide displays an ability to suppress the proliferation of polyclonally activated human T cells. Importantly, this suppressive effect was impaired in T cells obtained from MS patients having higher disability status. Therefore, it is plausible that progression of MS is associated with an escape from the immune-regulatory effect of sulfatide. Our study suggests that, although the precise mechanisms remain unrevealed, an escape of T cells from immunosuppression by sulfatide is associated with disease progression in the advanced stage. Further studies will provide novel insights into the pathogenesis of MS, particularly regarding disease progression, and help develop novel treatment strategies for this challenging disease.

Indexed as

Encephalomyelitis, Autoimmune, ExperimentalMultiple SclerosisAnimalsDisease ProgressionHumansImmunosuppression TherapyMiceSeverity of Illness IndexSulfoglycosphingolipidsT-LymphocytesSulfoglycosphingolipidsMultiple sclerosisMyelin glycolipidSulfatideT cells

Identifiers

PMID35689766
OpenAlexW4282927008

What OpenQuestion holds

Textmetadata
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.