Evidence map›Paper›PMID 19190179›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2009

Pituitary adenylyl cyclase-activating polypeptide is an intrinsic regulator of Treg abundance and protects against experimental autoimmune encephalomyelitis.

Yossan-Var Tan, Catalina Abad, Robert Lopez, Hongmei Dong, Shen Liu, Alice Lee, Rosa P Gomariz, Javier Leceta, James A Waschek

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 papers.

0numbers the graph read from it
0cells of the map it votes in
56citing papers in PubMed
3.7field-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

56 citing papers in PubMed, 99 citations in OpenAlex.

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  15. Immunomodulatory Roles of PACAP and VIP: Lessons from Knockout Mice.Journal of molecular neuroscience : MN · 2018
    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

9 authors at 2 institutions in 2 countries.

Yossan-Var TanSemel Institute/Department of Psychiatry, David Geffen School of Medicine, University of California, Los Angeles, CA 90095, USA.
Catalina Abad
Robert Lopez
Hongmei Dong
Shen Liu
Alice Lee
Rosa P Gomariz
Javier Leceta
James A Waschek
University of California, Los Angeles · USUniversidad Complutense de Madrid · ES

Funding

Stem CellsP30HD004612 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI BOOKHEIMER, SUSAN Y · 1985 to 2014
$19.5M
VIP AND PACP ACTION IN CNS DEVELOPMENT AND INJURYP01HD006576 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI DE VELLIS, JEAN · 1985 to 2006
$7.8M
NICHD NIH HHS HD04612NICHD NIH HHS HD06576NICHD NIH HHS P01 HD006576NICHD NIH HHS P30 HD004612
6 · The paper itself

Abstract

Pituitary adenylyl cyclase-activating polypeptide (PACAP) is a widely expressed neuropeptide originally discovered in the hypothalamus. It closely resembles vasoactive intestinal peptide (VIP), a neuropeptide well known to inhibit macrophage activity, promote Th2-type responses, and enhance regulatory T cell (Treg) production. Recent studies have shown that administration of PACAP, like VIP, can attenuate dramatically the clinical and pathological features of murine models of autoimmune diseases such as experimental autoimmune encephalomyelitis (EAE) and collagen-induced arthritis. However, specific roles (if any) of endogenous VIP and PACAP in the protection against autoimmune diseases have not been explored. Here, we subjected PACAP-deficient mice to myelin oligodendrocyte glycoprotein (MOG(35-55))-induced EAE. MOG immunization of PACAP-deficient mice triggered heightened clinical and pathological manifestations of EAE compared to wild-type mice. The increased sensitivity was accompanied by enhanced mRNA expression of proinflammatory cytokines (TNFalpha, IL-6, IFN-gamma, IL-12p35, IL-23p19, and IL-17), chemokines (MCP-1/CCL2, MIP-1alpha/CCL3, and RANTES/CCL5), and chemotactic factor receptors (CCR1, CCR2, and CCR5), but downregulation of the anti-inflammatory cytokines (IL-4, IL-10, and TGF-beta) in the spinal cord. Moreover, the abundance of CD4(+)CD25(+)FoxP3(+) Tregs in lymph nodes and levels of FoxP3 mRNA in the spinal cord were also diminished. The reduction in Tregs was associated with increased proliferation and decreased TGF-beta secretion in lymph node cultures stimulated with MOG. These results demonstrate that endogenous PACAP provides protection in EAE and identify PACAP as an intrinsic regulator of Treg abundance after inflammation.

Indexed as

AnimalsAutoimmune DiseasesCytokinesEncephalomyelitis, Autoimmune, ExperimentalGene Expression RegulationLymph NodesLymphocyte CountMiceMice, KnockoutMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsPituitary Adenylate Cyclase-Activating PolypeptideReceptors, CCRSpinal CordT-Lymphocytes, RegulatoryAdcyap1 protein, mouseCytokinesMog protein, mouseMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinMyelin ProteinsPituitary Adenylate Cyclase-Activating PolypeptideReceptors, CCRVasoactive Intestinal Peptide

Identifiers

PMID19190179
PMCPMC2644155
OpenAlexW2037522042

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.