ArticleDiabetes2016
Antigen Presentation and T-Cell Activation Are Critical for RBP4-Induced Insulin Resistance.
Article in Diabetes, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
What it found
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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.
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.
Who cites it
37 citing papers in PubMed, 68 citations in OpenAlex.
- Toll Like Receptor 4: A Potential Link Between Obesity and Metabolic Diseases.Obesity reviews : an official journal of the International Association for the Study of Obesity · 2026Review
- Adhesion-Related Macrophages Regulate Metabolic Homeostasis Through CAV-1 Dependency.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- RBP4 in Ageing.Biomedicines · 2026Review
- Retinol-binding protein 4 in cardiovascular diseases: mechanisms and therapeutic perspectives.Frontiers in cardiovascular medicine · 2026Review
- Optimization of Erythrocyte Lysis Protocols for Robust and Reproducible T Cell Analysis in Murine Peripheral Blood, Spleen, Lung, and Bone Marrow.Journal of immunology research · 2026Article
- Bioinformatics analyses of comorbid mechanisms between psoriasis and type 2 diabetes mellitus.Scientific reports · 2025Article
- Adipokines: masterminds of metabolic inflammation.Nature reviews. Immunology · 2025Review
- Retinol binding protein 4 and type 2 diabetes: from insulin resistance to pancreatic β-cell function.Endocrine · 2024Review
- RBP4 promotes denervation-induced muscle atrophy through STRA6-dependent pathway.Journal of cachexia, sarcopenia and muscle · 2024Article
- Adenosine and adenosine receptors in metabolic imbalance-related neurological issues.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2024Review
- The Hepatokine RBP4 Links Metabolic Diseases to Articular Inflammation.Antioxidants (Basel, Switzerland) · 2024Article
- Shift work is associated with an increased risk of type 2 diabetes and elevated RBP4 level: cross sectional analysis from the OHSPIW cohort study.BMC public health · 2023Article
- Friend or foe for obesity: How hepatokines remodel adipose tissues and translational perspective.Genes & diseases · 2023Review
- Serum retinol-binding protein 4 in stroke patients: correlation with T helper 17/regulatory T cell imbalance and 3-year cognitive function decline.Frontiers in neurology · 2023Article
- Interorgan communication with the liver: novel mechanisms and therapeutic targets.Frontiers in immunology · 2023Review
- Morbid Obesity in Women Is Associated with an Altered Intestinal Expression of Genes Related to Cancer Risk and Immune, Defensive, and Antimicrobial Response.Biomedicines · 2022Article
- Review
- Retinoid Homeostasis and Beyond: How Retinol Binding Protein 4 Contributes to Health and Disease.Nutrients · 2022Review
- Transcriptomic Analysis of Fish Hosts Responses to Nervous Necrosis Virus.Pathogens (Basel, Switzerland) · 2022Review
- Adipose tissue macrophages in remote modulation of hepatic glucose production.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Adipose tissue (AT) inflammation contributes to impaired insulin action, which is a major cause of type 2 diabetes. RBP4 is an adipocyte- and liver-derived protein with an important role in insulin resistance, metabolic syndrome, and AT inflammation. RBP4 elevation causes AT inflammation by activating innate immunity, which elicits an adaptive immune response. RBP4-overexpressing mice (RBP4-Ox) are insulin resistant and glucose intolerant and have increased AT macrophages and T-helper 1 cells. We show that high-fat diet-fed RBP4(-/-) mice have reduced AT inflammation and improved insulin sensitivity versus wild type. We also elucidate the mechanism for RBP4-induced macrophage antigen presentation and subsequent T-cell activation. In RBP4-Ox, AT macrophages display enhanced c-Jun N-terminal kinase, extracellular signal-related kinase, and p38 phosphorylation. Inhibition of these pathways and of NF-κB reduces activation of macrophages and CD4 T cells. MyD88 is an adaptor protein involved in proinflammatory signaling. In macrophages from MyD88(-/-) mice, RBP4 fails to stimulate secretion of tumor necrosis factor, IL-12, and IL-6 and CD4 T-cell activation. In vivo blockade of antigen presentation by treating RBP4-Ox mice with CTLA4-Ig, which blocks costimulation of T cells, is sufficient to reduce AT inflammation and improve insulin resistance. Thus, MyD88 and downstream mitogen-activated protein kinase and NF-κB pathways are necessary for RBP4-induced macrophage antigen presentation and subsequent T-cell activation. Also, blocking antigen presentation with CTLA4-Ig improves RBP4-induced insulin resistance and macrophage-induced T-cell activation.
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What OpenQuestion holds
Registered trials
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.