Evidence map›Paper›PMID 25305591›Full record

ArticleBrain, behavior, and immunity2015

VPAC2 (vasoactive intestinal peptide receptor type 2) receptor deficient mice develop exacerbated experimental autoimmune encephalomyelitis with increased Th1/Th17 and reduced Th2/Treg responses.

Yossan-Var Tan, Catalina Abad, Yuqi Wang, Robert Lopez, James Waschek

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Brain, behavior, and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
–field-weighted citation impact
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

30 citing papers in PubMed.

  1. Article
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  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Significance of serum VIP and PACAP in multiple sclerosis: an exploratory case-control study.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Review
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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

5 authors.

Yossan-Var Tan *Department of Psychiatry, David Geffen School of Medicine, University of California at Los Angeles, USA.
Catalina Abad *Department of Psychiatry, David Geffen School of Medicine, University of California at Los Angeles, USA.
Yuqi WangDepartment of Psychiatry, David Geffen School of Medicine, University of California at Los Angeles, USA.
Robert LopezDepartment of Psychiatry, David Geffen School of Medicine, University of California at Los Angeles, USA.
James WaschekDepartment of Psychiatry, David Geffen School of Medicine, University of California at Los Angeles, USA.

Funding

Women's CancersP30CA016042 · NCI · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI Samuel Wheeler French · 1985 to 2026
$134.5M
Stem CellsP30HD004612 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOOKHEIMER, SUSAN Y · 1985 to 2014
$19.5M
Pilot and Feasibility ProgramP30DK041301 · NIDDK · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ROZENGURT, JUAN ENRIQUE · 1990 to 2019
$18.0M
NCI NIH HHS P30 CA016042NICHD NIH HHS HD04612NICHD NIH HHS P30 HD004612NIDDK NIH HHS P30 DK041301
6 · The paper itself

Abstract

Vasoactive intestinal peptide (VIP) and pituitary adenylyl cyclase-activating polypeptide (PACAP) are two structurally-related neuropeptides with widespread expression in the central and peripheral nervous systems. Although these peptides have been repeatedly shown to exert potent anti-inflammatory actions when administered in animal models of inflammatory disease, mice deficient in VIP and PACAP were recently shown to exhibit different phenotypes (ameliorated and exacerbated, respectively) in response to experimental autoimmune encephalomyelitis (EAE). Therefore, elucidating what are the specific immunoregulatory roles played by each of their receptor subtypes (VPAC1, VPAC2, and PAC1) is critical. In this study, we found that mice with a genetic deletion of VIPR2, encoding the VPAC2 receptor, exhibited exacerbated (MOG35-55)-induced EAE compared to wild type mice, characterized by enhanced clinical and histopathological features, increased proinflammatory cytokines (TNF-α, IL-6, IFN-γ (Th1), and IL-17 (Th17)) and reduced anti-inflammatory cytokines (IL-10, TGFβ, and IL-4 (Th2)) in the CNS and lymph nodes. Moreover, the abundance and proliferative index of lymph node, thymus and CNS CD4(+)CD25(+)FoxP3(+) Tregs were strikingly reduced in VPAC2-deficient mice with EAE. Finally, the in vitro suppressive activity of lymph node and splenic Tregs from VPAC2-deficient mice was impaired. Overall, our results demonstrate critical protective roles for PACAP and the VPAC2 receptor against autoimmunity, promoting the expansion and maintenance of the Treg pool.

Indexed as

AnimalsCell ProliferationEncephalomyelitis, Autoimmune, ExperimentalGene ExpressionInterferon-gammaInterleukin-17Interleukin-4MiceMice, Inbred C57BLMice, KnockoutReceptors, Vasoactive Intestinal Peptide, Type IIRNA, MessengerSpinal CordT-Lymphocytes, RegulatoryInterferon-gammaInterleukin-17Interleukin-4Receptors, Vasoactive Intestinal Peptide, Type IIRNA, MessengerAutoimmunityExperimental autoimmune encephalomyelitisInflammationNeuroimmunologyNeuropeptideRegulatory T cellVPAC2 receptor

Identifiers

PMID25305591
PMCPMC4275378

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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.