Evidence map›Paper›PMID 28325905›Full record

ArticleScientific reports2017

Evidence for C1q-mediated crosslinking of CD33/LAIR-1 inhibitory immunoreceptors and biological control of CD33/LAIR-1 expression.

Myoungsun Son, Betty Diamond, Bruce T Volpe, Cynthia B Aranow, Meggan C Mackay, Frances Santiago-Schwarz

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

38 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  7. Adaptation and conservation of CL-10/11 in avian lungs: implications for their role in pulmonary innate immune protection.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2025
    Article
  8. Review
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  10. The Complement System.Advances in experimental medicine and biology · 2025
    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

6 authors at 1 institution in 1 country.

Myoungsun SonCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, 11030, USA.ORCID 0000-0002-0655-3859
Betty DiamondCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, 11030, USA.
Bruce T VolpeCenter for Biomedical Science, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, 11030, USA.
Cynthia B AranowCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, 11030, USA.
Meggan C MackayCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, 11030, USA.
Frances Santiago-SchwarzCenter for Autoimmune and Musculoskeletal Diseases, The Feinstein Institute for Medical Research, Northwell Health, Manhasset, NY, 11030, USA. Fsantiago1@northwell.edu.ORCID 0000-0001-9393-327X
Northwell Health · US

Funding

Targeting cognitive and immune impairment in sepsis survivorsP01AI102852 · NIAID · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI TRACEY, KEVIN J · 2014 to 2018
$11.5M
Regulation of LAIR-1 in LupusK01AR065506 · NIAMS · FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH · PI SON, MYOUNGSUN · 2014 to 2018
$639k
NIAID NIH HHS P01 AI102852NIAMS NIH HHS K01 AR065506
6 · The paper itself

Abstract

C1q collagen-like region (CLR) engaging and activating the LAIR-1 inhibitory immunoreceptor represents a non-complement mechanism for maintaining immune quiescence. Given the binding promiscuity of C1q's globular region (gC1q), we hypothesized that C1q concurrently associates with distinct inhibitory immunoreceptors to produce C1q-mediated modulatory networking. Like LAIR-1, CD33 inhibitory immunoreceptors are highly expressed on monocytes. Binding CD33 restricts cell activation/differentiation; however, natural ligands for CD33 remain elusive. CD33 has IgC2-like domains potentially recognized by gC1q. Thus, we asked whether C1q binds to CD33 and if C1q mediates CD33/LAIR-1 crosslinking. Our findings demonstrate that C1q and gC1q interact with CD33 to activate its inhibitory motifs, while CLR does not. Whole C1q is required to crosslink CD33 and LAIR-1 and concurrently activate CD33/LAIR-1 inhibitory motifs. While C1q binds CD33C2 domains, decreased C1q-CD33 interactions resulting from sialic acid masking of CD33C2 domains suggests a process for regulating C1q-CD33 activity. Consistent with defective self-tolerance, CD33/LAIR-1 expression is reduced in systemic lupus erythematosus (SLE) myelomonocytes. The anti-inflammatory cytokine M-CSF, but not DC growth factors, sustains CD33/LAIR-1 expression on both healthy and SLE cells suggesting further biological control of C1q-CD33/LAIR-1 processes.

Indexed as

Cells, CulturedComplement C1qGene ExpressionHumansProtein BindingReceptors, ImmunologicSialic Acid Binding Ig-like Lectin 3CD33 protein, humanComplement C1qleukocyte-associated immunoglobulin-like receptor 1Receptors, ImmunologicSialic Acid Binding Ig-like Lectin 3

Identifiers

PMID28325905
PMCPMC5412647
OpenAlexW2603824203

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.