Evidence map›Paper›PMID 21647172›Full record

ArticleImmunology and cell biology2012

SAP suppresses the development of experimental autoimmune encephalomyelitis in C57BL/6 mice.

Zhe Ji, Zun-Ji Ke, Jian-Guo Geng

Abstract read
In one paragraph

Article in Immunology and cell biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

16 citing papers in PubMed, 26 citations in OpenAlex.

  1. Article
  2. Inhibitors of the Sialidase NEU3 as Potential Therapeutics for Fibrosis.International journal of molecular sciences · 2022
    Review
  3. Article
  4. Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Review
  10. Article
  11. Article
  12. Janus faces of amyloid proteins in neuroinflammation.Journal of clinical immunology · 2014
    Review
  13. Article
  14. New approaches to modulating idiopathic pulmonary fibrosis.Current allergy and asthma reports · 2013
    Review
  15. Article
  16. Host responses in tissue repair and fibrosis.Annual review of pathology · 2013
    Review
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

3 authors at 2 institutions in 1 country.

Zhe JiLaboratory of Molecular Cell Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. jizhe2008@gmail.com
Zun-Ji Ke
Jian-Guo Geng
Chinese Academy of Sciences · CNCenter for Excellence in Molecular Cell Science · CN

Funding

Modulation of Leukocyte Adhesion by P-selectin/PSGL-1 SignalingR01AI064743 · NIAID · UNIVERSITY OF MINNESOTA · PI GENG, JIAN-GUO · 2007 to 2011
$1.8M
Slit-Robo Signaling in Tumor Growth and MetastasisR01CA126897 · NCI · UNIVERSITY OF MINNESOTA · PI GENG, JIAN-GUO · 2009 to 2013
$1.5M
NCI NIH HHS R01 CA126897NIAID NIH HHS R01 AI064743
6 · The paper itself

Abstract

Experimental autoimmune encephalomyelitis (EAE) is a CD4(+) T cell-mediated disease of the central nervous system. Serum amyloid P component (SAP) is a highly conserved plasma protein named for its universal presence in amyloid deposits. Here we report that SAP-transgenic mice had unexpectedly attenuated EAE due to impaired encephalitogenic responses. Following induction with myelin oligodendroglial glycoprotein (MOG) peptide 35-55 in complete Freund's adjuvant, SAP-transgenic mice showed reduced spinal cord inflammation with lower severity of EAE attacks as compared with control C57BL/6 mice. However, in SAP-Knockout mice, the severity of EAE is enhanced. Adoptive transfer of Ag-restimulated T cells from wild type to SAP-transgenic mice, or transfer of SAP-transgenic Ag-restimulated T cells to control mice, induced milder EAE. T cells from MOG-primed SAP-transgenic mice showed weak proliferative responses. Furthermore, in SAP-transgenic mice, there is little infiltration of CD45-positive cells in the spinal cord. In vitro, SAP suppressed the secretion of interleukin-2 stimulated by P-selectin and blocked P-selectin binding to T cells. Moreover, SAP could change the affinity between α4-integrin and T cells. These data suggested that SAP could antagonize the development of the acute phase of inflammation accompanying EAE by modulating the function of P-selectin.

Indexed as

Adoptive TransferAnimalsEncephalomyelitis, Autoimmune, ExperimentalInflammationIntegrin alpha4MiceMice, Inbred C57BLMice, KnockoutMice, TransgenicP-SelectinSerum Amyloid P-ComponentT-LymphocytesIntegrin alpha4P-SelectinSerum Amyloid P-Component

Identifiers

PMID21647172
PMCPMC3880774
OpenAlexW1965799141

What OpenQuestion holds

Textmetadata
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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.