Evidence map›Paper›PMID 26077779›Full record

ArticleJournal of neuroinflammation2015

Interleukin-22 is increased in multiple sclerosis patients and targets astrocytes.

Guillaume Perriard, Amandine Mathias, Lukas Enz, Mathieu Canales, Myriam Schluep, Melanie Gentner, Nicole Schaeren-Wiemers, Renaud A Du Pasquier

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 65 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
65citing papers in PubMed, 1 pooled it
4.2field-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

65 citing papers in PubMed, 1 synthesis or guideline pooled it, 110 citations in OpenAlex.

  1. Pooled it
  2. Regulatory T cells attenuate astrogliosis via IL-10/STAT3/PKC/vimentin signaling and promote neurological recovery after spinal cord injury.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026
    Article
  3. Article
  4. Article
  5. Review
  6. Review
  7. Article
  8. Article
  9. Differentiation and regulation of CD4Cellular and molecular life sciences : CMLS · 2024
    Review
  10. Article
  11. Review
  12. Review
  13. Plasma proteomic profiles of UK Biobank participants with multiple sclerosis.Annals of clinical and translational neurology · 2024
    Article
  14. Article
  15. Article
  16. Review
  17. Review
  18. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  19. Article
  20. Article

5 more citing papers are in PubMed but not listed here.

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

8 authors at 2 institutions in 1 country.

Guillaume PerriardLaboratory of Neuroimmunology, Center of Research in Neurosciences, Department of Clinical Neurosciences and Service of Immunology and Allergy, Department of Medicine, CHUV, 1011, Lausanne, Switzerland.
Amandine MathiasLaboratory of Neuroimmunology, Center of Research in Neurosciences, Department of Clinical Neurosciences and Service of Immunology and Allergy, Department of Medicine, CHUV, 1011, Lausanne, Switzerland.
Lukas EnzNeurobiology, Department of Biomedicine, University Hospital Basel, University of Basel, 4031, Basel, Switzerland.
Mathieu CanalesLaboratory of Neuroimmunology, Center of Research in Neurosciences, Department of Clinical Neurosciences and Service of Immunology and Allergy, Department of Medicine, CHUV, 1011, Lausanne, Switzerland.
Myriam SchluepService of Neurology, Department of Clinical Neurosciences, CHUV BH-10/131, 46, rue du Bugnon, 1011, Lausanne, Switzerland.
Melanie GentnerNeurobiology, Department of Biomedicine, University Hospital Basel, University of Basel, 4031, Basel, Switzerland.
Nicole Schaeren-WiemersNeurobiology, Department of Biomedicine, University Hospital Basel, University of Basel, 4031, Basel, Switzerland.
Renaud A Du PasquierLaboratory of Neuroimmunology, Center of Research in Neurosciences, Department of Clinical Neurosciences and Service of Immunology and Allergy, Department of Medicine, CHUV, 1011, Lausanne, Switzerland. renaud.du-pasquier@chuv.ch.
University Hospital of Basel · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreasing evidences link T helper 17 (Th17) cells with multiple sclerosis (MS). In this context, interleukin-22 (IL-22), a Th17-linked cytokine, has been implicated in blood brain barrier breakdown and lymphocyte infiltration. Furthermore, polymorphism between MS patients and controls has been recently described in the gene coding for IL-22 binding protein (IL-22BP). Here, we aimed to better characterize IL-22 in the context of MS.

methodsIL-22 and IL-22BP expressions were assessed by ELISA and qPCR in the following compartments of MS patients and control subjects: (1) the serum, (2) the cerebrospinal fluid, and (3) immune cells of peripheral blood. Identification of the IL-22 receptor subunit, IL-22R1, was performed by immunohistochemistry and immunofluorescence in human brain tissues and human primary astrocytes. The role of IL-22 on human primary astrocytes was evaluated using 7-AAD and annexin V, markers of cell viability and apoptosis, respectively.

resultsIn a cohort of 141 MS patients and healthy control (HC) subjects, we found that serum levels of IL-22 were significantly higher in relapsing MS patients than in HC but also remitting and progressive MS patients. Monocytes and monocyte-derived dendritic cells contained an enhanced expression of mRNA coding for IL-22BP as compared to HC. Using immunohistochemistry and confocal microscopy, we found that IL-22 and its receptor were detected on astrocytes of brain tissues from both control subjects and MS patients, although in the latter, the expression was higher around blood vessels and in MS plaques. Cytometry-based functional assays revealed that addition of IL-22 improved the survival of human primary astrocytes. Furthermore, tumor necrosis factor α-treated astrocytes had a better long-term survival capacity upon IL-22 co-treatment. This protective effect of IL-22 seemed to be conferred, at least partially, by a decreased apoptosis.

conclusionsWe show that (1) there is a dysregulation in the expression of IL-22 and its antagonist, IL-22BP, in MS patients, (2) IL-22 targets specifically astrocytes in the human brain, and (3) this cytokine confers an increased survival of the latter cells.

Indexed as

AdultAgedAged, 80 and overApoptosisAstrocytesBrainCase-Control StudiesCells, CulturedCell SurvivalFemaleHumansInterleukin-22InterleukinsMaleMiddle AgedMultiple SclerosisIL22RA2 protein, humanInterleukin-22InterleukinsReceptors, InterleukinTumor Necrosis Factor-alpha

Identifiers

PMID26077779
PMCPMC4480507
OpenAlexW1570269285

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LicenceCC BY
Read underepoch 390

Registered trials

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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.