Evidence map›Paper›PMID 22184635›Full record

ArticleThe Journal of experimental medicine2012

High-mobility group nucleosome-binding protein 1 acts as an alarmin and is critical for lipopolysaccharide-induced immune responses.

De Yang, Yuri V Postnikov, Yana Li, Poonam Tewary, Gonzalo de la Rosa, Feng Wei, Dennis Klinman, Theresa Gioannini, Jerrold P Weiss, Takashi Furusawa and 2 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
4.4field-weighted citation impact, top 5% 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

90 citing papers in PubMed, 149 citations in OpenAlex.

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  12. Do Alarmins Have a Role in Multiple Myeloma?Turkish journal of haematology : official journal of Turkish Society of Haematology · 2024
    Article
  13. Article
  14. Article
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  16. Review
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30 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

12 authors at 6 institutions in 2 countries.

De YangBasic Research Program, Scientific Application and International Corporation–Frederick, Inc, Frederick, Frederick, MD 21702, USA. yangd@mail.nih.gov
Yuri V Postnikov
Yana Li
Poonam Tewary
Gonzalo de la Rosa
Feng Wei
Dennis Klinman
Theresa Gioannini
Jerrold P Weiss
Takashi Furusawa
Michael Bustin
Joost J Oppenheim
Laboratory of Molecular Genetics · PLNational Cancer Institute · USFrederick National Laboratory for Cancer Research · USUniversity of Iowa · USNational Institutes of Health · USScience Applications International Corporation (United States) · US

Funding

Studies of Receptor Interactions and Effects of AlarminsZIABC009369 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI OPPENHEIM, JOOST J · 2009 to 2022
$16.5M
Mechanism of action and therapeutic utility of stimulatory CpG oligonucleotidesZIABC010852 · NCI · DIVISION OF BASIC SCIENCES - NCI · PI KLINMAN, DENNIS · 2009 to 2019
$11.3M
Regulation of MD-2 function and expressionR01AI059372 · NIAID · UNIVERSITY OF IOWA · PI WEISS, JERROLD P · 2004 to 2013
$3.6M
CCR NIH HHS HHSN261200800001CIntramural NIH HHSNCI NIH HHS HHSN261200800001ENIAID NIH HHS R01 AI059372
6 · The paper itself

Abstract

Alarmins are endogenous mediators capable of promoting the recruitment and activation of antigen-presenting cells (APCs), including dendritic cells (DCs), that can potentially alert host defense against danger signals. However, the relevance of alarmins to the induction of adaptive immune responses remains to be demonstrated. In this study, we report the identification of HMGN1 (high-mobility group nucleosome-binding protein 1) as a novel alarmin and demonstrate that it contributes to the induction of antigen-specific immune responses. HMGN1 induced DC maturation via TLR4 (Toll-like receptor 4), recruitment of APCs at sites of injection, and activation of NF-κB and multiple mitogen-activated protein kinases in DCs. HMGN1 promoted antigen-specific immune response upon co-administration with antigens, and Hmgn1(-/-) mice developed greatly reduced antigen-specific antibody and T cell responses when immunized with antigens in the presence of lipopolysaccharide (LPS). The impaired ability of Hmgn1(-/-) mice to mount antigen-specific immune responses was accompanied by both deficient DC recruitment at sites of immunization and reduced production of inflammatory cytokines. Bone marrow chimera experiments revealed that HMGN1 derived from nonleukocytes was critical for the induction of antigen-specific antibody and T cell responses. Thus, extracellular HMGN1 acts as a novel alarmin critical for LPS-induced development of innate and adaptive immune responses.

Indexed as

ImmunityAdaptor Proteins, Vesicular TransportAnimalsAntigensCell DifferentiationCell LineDendritic CellsFemaleHEK293 CellsHMGN1 ProteinHumansImmunity, InnateLipopolysaccharidesMaleMiceMice, Inbred C57BLAdaptor Proteins, Vesicular TransportAntigensHMGN1 ProteinLipopolysaccharidesMyeloid Differentiation Factor 88Toll-Like Receptor 4

Identifiers

PMID22184635
PMCPMC3260868
OpenAlexW2129751113

What Socratic holds

Textmetadata
LicenceCC BY-NC-SA
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 Socratic graph.