Evidence map›Paper›PMID 36867536›Full record

ArticleCell reports2023

CD169+ macrophage intrinsic IL-10 production regulates immune homeostasis during sepsis.

Stephen T Yeung, Luis J Ovando, Ashley J Russo, Vijay A Rathinam, Kamal M Khanna

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
9.4field-weighted citation impact, top 2% 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

51 citing papers in PubMed, 57 citations in OpenAlex.

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  5. Type I interferon-induced CD169Journal of periodontology · 2026
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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 at 3 institutions in 1 country.

Stephen T YeungDepartment of Microbiology, New York University Langone School of Medicine, New York, NY 10016, USA.
Luis J OvandoDepartment of Microbiology, New York University Langone School of Medicine, New York, NY 10016, USA.
Ashley J RussoDepartment of Immunology, UConn Health School of Medicine, Farmington, CT 06032, USA.
Vijay A RathinamDepartment of Immunology, UConn Health School of Medicine, Farmington, CT 06032, USA.
Kamal M KhannaDepartment of Microbiology, New York University Langone School of Medicine, New York, NY 10016, USA; Perlmutter Cancer Center, New York University Langone Health, New York, NY 10016, USA. Electronic address: kamal.khanna@nyulangone.org.
New York University · USUConn Health · USNYU Langone Health · US

Funding

Vaccine FacilityP30CA016087 · NCI · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI ANIRBAN MAITRA · 1985 to 2026
$83.1M
Novel lung resident interstitial macrophage subset with distinct localization and polarizationR01AI143861 · NIAID · NEW YORK UNIVERSITY SCHOOL OF MEDICINE · PI KHANNA, KAMAL MOHAN · 2019 to 2023
$3.3M
NCI NIH HHS P30 CA016087NIAID NIH HHS R01 AI143861
6 · The paper itself

Abstract

Macrophages facilitate critical functions in regulating pathogen clearance and immune homeostasis in tissues. The remarkable functional diversity exhibited by macrophage subsets is dependent on tissue environment and the nature of the pathological insult. Our current knowledge of the mechanisms that regulate the multifaceted counter-inflammatory responses mediated by macrophages remains incomplete. Here, we report that CD169+ macrophage subsets are necessary for protection under excessive inflammatory conditions. We show that in the absence of these macrophages, even under mild septic conditions, mice fail to survive and exhibit increased production of inflammatory cytokines. Mechanistically, CD169+ macrophages control inflammatory responses via interleukin-10 (IL-10), as CD169+ macrophage-specific deletion of IL-10 was lethal during septic conditions, and recombinant IL-10 treatment reduced lipopolysaccharide (LPS)-induced lethality in mice lacking CD169+ macrophages. Collectively, our findings show a pivotal homeostatic role for CD169+ macrophages and suggest they may serve as an important target for therapy under damaging inflammatory conditions.

Indexed as

Interleukin-10SepsisAnimalsCytokinesLipopolysaccharidesMacrophagesMiceSialic Acid Binding Ig-like Lectin 1CytokinesIL10 protein, mouseInterleukin-10LipopolysaccharidesSialic Acid Binding Ig-like Lectin 1Siglec1 protein, mouseCD169CP: ImmunologyG-CSFIL-10LPSmacrophagesseptic shockSiglec-1

Identifiers

PMID36867536
PMCPMC10123955
OpenAlexW4322772807

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.