Evidence map›Paper›PMID 29871859›Full record

ArticleDiabetes2018

TACI-Deficient Macrophages Protect Mice Against Metaflammation and Obesity-Induced Dysregulation of Glucose Homeostasis.

Lunhua Liu, Karen Etsuko Inouye, Windy Rose Allman, Adam Steven Coleman, Shafiuddin Siddiqui, Gökhan Siddik Hotamisligil, Mustafa Akkoyunlu

Open access · bronzeAbstract readComparative Study
PubMed Full text at PMC Publisher
In one paragraph

Article in Diabetes, 2018. 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
1.8field-weighted citation impact, top 15% 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, 21 citations in OpenAlex.

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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

7 authors at 1 institution in 1 country.

Lunhua LiuLaboratory of Bacterial Polysaccharides, Division of Bacterial Parasitic and Allergenic Products, U.S. Food and Drug Administration, Silver Spring, MD.
Karen Etsuko InouyeDepartment of Genetics and Complex Diseases and Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA.
Windy Rose AllmanLaboratory of Bacterial Polysaccharides, Division of Bacterial Parasitic and Allergenic Products, U.S. Food and Drug Administration, Silver Spring, MD.
Adam Steven ColemanLaboratory of Bacterial Polysaccharides, Division of Bacterial Parasitic and Allergenic Products, U.S. Food and Drug Administration, Silver Spring, MD.
Shafiuddin SiddiquiLaboratory of Bacterial Polysaccharides, Division of Bacterial Parasitic and Allergenic Products, U.S. Food and Drug Administration, Silver Spring, MD.
Gökhan Siddik HotamisligilDepartment of Genetics and Complex Diseases and Sabri Ülker Center, Harvard T.H. Chan School of Public Health, Boston, MA.
Mustafa AkkoyunluLaboratory of Bacterial Polysaccharides, Division of Bacterial Parasitic and Allergenic Products, U.S. Food and Drug Administration, Silver Spring, MD mustafa.akkoyunlu@fda.hhs.gov.ORCID 0000-0001-9958-4031
United States Food and Drug Administration · US

Funding

TNF RECEPTOR FUNCTION IN INSULIN RESISTANCE AND OBESITYR01DK052539 · NIDDK · HARVARD UNIVERSITY (SCH OF PUBLIC HLTH) · PI HOTAMISLIGIL, GOKHAN S · 1998 to 2017
$6.8M
The role of immunometabolic pathways in atherosclerosisR01HL125753 · NHLBI · HARVARD SCHOOL OF PUBLIC HEALTH · PI HOTAMISLIGIL, GOKHAN S · 2015 to 2018
$1.6M
NHLBI NIH HHS R01 HL125753NIDDK NIH HHS R01 DK052539
6 · The paper itself

Abstract

Transmembrane activator and calcium modulator and cyclophilin ligand interactor (TACI) is a receptor for the TNF superfamily cytokines, B cell-activating factor (BAFF), and A proliferation-inducing ligand (APRIL). Here, we demonstrate that TACI-deficient mice subjected to high-fat diet (HFD) are protected from weight gain and dysregulated glucose homeostasis. Resistance to HFD-induced metabolic changes in TACI-deficient mice does not involve TACI-mediated adipogenesis. Instead, accumulation of M2 macrophages (Mϕs), eosinophils, and type 2 innate lymphoid cells in visceral adipose tissue (VAT) is implicated in the protection from obesity-induced assaults. In support of this hypothesis, adoptively transferred TACI-deficient peritoneal or adipose tissue Mϕs, but not B cells, can improve glucose metabolism in the obese host. Interestingly, the transferred TACI-deficient Mϕs not only home to host VAT but also trigger the accumulation of host M2 Mϕs and eosinophils in VAT. The increase in host M2 Mϕs in VAT is likely a result of eosinophil recruitment in response to eotaxin-2 produced by TACI-deficient Mϕs. Insulin signaling experiments revealed that IL-10 secreted by TACI-deficient Mϕs is responsible for maintaining adipocyte insulin sensitivity. Thus, the adoptive transfer experiments offer a model where TACI-deficient Mϕs accumulate in VAT and protect against metaflammation and obesity-associated dysregulation of glucose metabolism.

Indexed as

AdiposityImmunotherapy, AdoptiveAnimalsBiomarkersCells, CulturedDiet, High-FatFemaleGene Expression RegulationGlucose IntoleranceInflammation MediatorsInsulin ResistanceIntra-Abdominal FatMacrophagesMacrophages, PeritonealMiceMice, KnockoutBiomarkersInflammation MediatorsTnfrsf13b protein, mouseTransmembrane Activator and CAML Interactor Protein

Identifiers

PMID29871859
PMCPMC6054430
OpenAlexW2806631886

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.