Evidence map›Paper›PMID 25753260›Full record

ArticleClinical and experimental immunology2015

Thymic stromal lymphopoietin deficiency attenuates experimental autoimmune encephalomyelitis.

J Eckhardt, M Döbbeler, C König, K Kuczera, C Kuhnt, C Ostalecki, E Zinser, T W Mak, A Steinkasserer, M Lechmann

Open access · bronzeAbstract read
In one paragraph

Article in Clinical and experimental immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
0.3field-weighted citation impact, top 35% 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

8 citing papers in PubMed, 13 citations in OpenAlex.

  1. IL-7Rα on CD4Journal of neuroinflammation · 2024
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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

10 authors at 2 institutions in 2 countries.

J EckhardtDepartment of Immune Modulation at the Department of Dermatology.
M DöbbelerDepartment of Immune Modulation at the Department of Dermatology.
C KönigDepartment of Immune Modulation at the Department of Dermatology.
K KuczeraDepartment of Immune Modulation at the Department of Dermatology.
C KuhntDepartment of Immune Modulation at the Department of Dermatology.
C OstaleckiDepartment of Dermatology, University Hospital Erlangen, Erlangen, Germany.
E ZinserDepartment of Immune Modulation at the Department of Dermatology.
T W MakThe Campbell Family Institute for Breast Cancer Research at Princess Margaret Hospital, University Health Network, Toronto, Ontario, Canada.
A SteinkassererDepartment of Immune Modulation at the Department of Dermatology.
M LechmannDepartment of Immune Modulation at the Department of Dermatology.
Universitätsklinikum Erlangen · DEUniversity Health Network · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In the present study we examined the role of thymic stromal lymphopoietin (TSLP) in experimental autoimmune encephalomyelitis (EAE). Here, we report that TSLP knock-out (KO) mice display a delayed onset of disease and an attenuated form of EAE. This delayed onset was accompanied by a reduced number of encephalitogenic T helper type 1 (Th1) cells in the central nervous system (CNS) of TSLP KO mice. In addition, CD4(+) and CD8(+) T cells from CNS of TSLP KO mice show a reduced activation status in comparison to wild-type mice. It is noteworthy that we could also show that lymph node cells from TSLP KO mice expanded less efficiently and that interleukin (IL)-6-, interferon (IFN)-γ and tumour necrosis factor (TNF)-α levels were reduced. Furthermore, CD3(+) T cells isolated in the preclinical phase from myelin oligodendrocyte glycoprotein peptide 35-55 (MOG(35-55))-immunized TSLP KO mice showed a reduced response after secondary exposure to MOG(35-55), indicating that differentiation of naive T cells into MOG(35-55)-specific effector and memory T cells was impaired in KO mice. The addition of recombinant TSLP enhanced T cell proliferation during MOG(35-55) restimulation, showing that T cells also respond directly to TSLP. In summary, these data demonstrate that expression of, and immune activation by, TSLP contributes significantly to the immunopathology of EAE.

Indexed as

AnimalsBone Marrow CellsCD8-Positive T-LymphocytesCell ProliferationCells, CulturedCentral Nervous SystemCytokinesEncephalomyelitis, Autoimmune, ExperimentalInflammationInterferon-gammaInterleukin-6Lymphocyte ActivationMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutCytokinesInterferon-gammaInterleukin-6Myelin-Oligodendrocyte Glycoproteinmyelin oligodendrocyte glycoprotein (35-55)Peptide FragmentsThymic Stromal LymphopoietinTSLP protein, mouseTumor Necrosis Factor-alphaautoimmunityEAET cellsTSLP

Identifiers

PMID25753260
PMCPMC4469155
OpenAlexW2062641590

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.