Evidence map›Paper›PMID 24966328›Full record

ArticleThe Journal of biological chemistry2014

CD1d-mediated presentation of endogenous lipid antigens by adipocytes requires microsomal triglyceride transfer protein.

Maryam Rakhshandehroo, Sanne M W Gijzel, Rasmus Siersbæk, Marjoleine F Broekema, Colin de Haar, Henk S Schipper, Marianne Boes, Susanne Mandrup, Eric Kalkhoven

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
1.7field-weighted citation impact, top 16% 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

26 citing papers in PubMed, 39 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

9 authors at 4 institutions in 3 countries.

Maryam RakhshandehrooFrom the Molecular Cancer Research, Center for Molecular Medicine and.
Sanne M W GijzelFrom the Molecular Cancer Research, Center for Molecular Medicine and.
Rasmus Siersbækthe Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense, Denmark.
Marjoleine F BroekemaFrom the Molecular Cancer Research, Center for Molecular Medicine and.
Colin de Haarthe Department of Pediatric Immunology, University Medical Center Utrecht, 3584 CG Utrecht, the Netherlands and.
Henk S SchipperFrom the Molecular Cancer Research, Center for Molecular Medicine and the Department of Pediatric Immunology, University Medical Center Utrecht, 3584 CG Utrecht, the Netherlands and.
Marianne Boesthe Department of Pediatric Immunology, University Medical Center Utrecht, 3584 CG Utrecht, the Netherlands and.
Susanne Mandrupthe Department of Biochemistry and Molecular Biology, University of Southern Denmark, DK-5230 Odense, Denmark.
Eric KalkhovenFrom the Molecular Cancer Research, Center for Molecular Medicine and e.kalkhoven@umcutrecht.nl.
Center for Molecular Medicine and Immunology · USCentro de Investigación del Cáncer · ESUtrecht University · NLUniversity Medical Center Utrecht · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Obesity-induced adipose tissue (AT) dysfunction results in a chronic low-grade inflammation that predisposes to the development of insulin resistance and type 2 diabetes. During the development of obesity, the AT-resident immune cell profile alters to create a pro-inflammatory state. Very recently, CD1d-restricted invariant (i) natural killer T (NKT) cells, a unique subset of lymphocytes that are reactive to so called lipid antigens, were implicated in AT homeostasis. Interestingly, recent data also suggest that human and mouse adipocytes can present such lipid antigens to iNKT cells in a CD1d-dependent fashion, but little is known about the lipid antigen presentation machinery in adipocytes. Here we show that CD1d, as well as the lipid antigen loading machinery genes pro-saposin (Psap), Niemann Pick type C2 (Npc2), α-galactosidase (Gla), are up-regulated in early adipogenesis, and are transcriptionally controlled by CCAAT/enhancer-binding protein (C/EBP)-β and -δ. Moreover, adipocyte-induced Th1 and Th2 cytokine release by iNKT cells also occurred in the absence of exogenous ligands, suggesting the display of endogenous lipid antigen-D1d complexes by 3T3-L1 adipocytes. Furthermore, we identified microsomal triglyceride transfer protein, which we show is also under the transcriptional regulation of C/EBPβ and -δ, as a novel player in the presentation of endogenous lipid antigens by adipocytes. Overall, our findings indicate that adipocytes can function as non-professional lipid antigen presenting cells, which may present an important aspect of adipocyte-immune cell communication in the regulation of whole body energy metabolism and immune homeostasis.

Indexed as

Antigen Presentation3T3-L1 CellsAdipocytesAdipogenesisAnimalsAntigens, CD1dCarrier ProteinsCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding Protein-deltaCell CommunicationEnergy MetabolismGene ExpressionGene Knockdown TechniquesHumansLipidsMiceAntigens, CD1dCarrier ProteinsCCAAT-Enhancer-Binding Protein-betaCCAAT-Enhancer-Binding Protein-deltaCebpb protein, mouseCebpd protein, mouseLipidsmicrosomal triglyceride transfer proteinAdipocyteAdipose Tissue MetabolismAntigen PresentationCCAAT-Enhancer-binding Protein (C/EBP)Lipid

Identifiers

PMID24966328
PMCPMC4139226
OpenAlexW2088714117

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.