ArticleInternational journal of obesity (2005)2015
CD28 deletion improves obesity-induced liver steatosis but increases adiposity in mice.
Article in International journal of obesity (2005), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 15 citations in OpenAlex.
- Immune checkpoints and immunoregulation in metabolic diseases and cancers: pathological mechanisms and therapeutic potential.Signal transduction and targeted therapy · 2026Review
- Immune crosstalk in metabolic dysfunction-associated steatotic liver disease: interactions between innate and adaptive immunity.Frontiers in immunology · 2026Review
- Mechanisms of Innate Immune Modulation by High-Fat Diet: Implications for Obesity and Asthma.Current allergy and asthma reports · 2025Review
- The bidirectional immune crosstalk in metabolic dysfunction-associated steatotic liver disease.Cell metabolism · 2023Review
- Dynamic chromatin architecture of the porcine adipose tissues with weight gain and loss.Nature communications · 2023Article
- Investigation of candidate genes and mechanisms underlying obesity associated type 2 diabetes mellitus using bioinformatics analysis and screening of small drug molecules.BMC endocrine disorders · 2021Article
- Obesity-induced inflammation and insulin resistance: A mini-review on T-cells.Metabolism open · 2019Article
- Qianggan extract improved nonalcoholic steatohepatitis by modulating lncRNA/circRNA immune ceRNA networks.BMC complementary and alternative medicine · 2019Article
- T Cells in Adipose Tissue: Critical Players in Immunometabolism.Frontiers in immunology · 2018Review
- The Cell Surface Markers Expression in Postmenopausal Women and Relation to Obesity and Bone Status.International journal of environmental research and public health · 2017Article
- Liver inflammation and fibrosis.The Journal of clinical investigation · 2017Review
- The role of immune cells in metabolism-related liver inflammation and development of non-alcoholic steatohepatitis (NASH).Reviews in endocrine & metabolic disorders · 2016Review
Corrections and comments
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Authors and funding
13 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND/
objectivesLymphocytes have a critical role in visceral adipose tissue (AT) inflammation. The CD28 costimulatory molecule is required for lymphocyte activation and for the development of a functional regulatory T cells (Tregs) compartment; however, its role during obesity is unknown.
methodsDuring diet-induced obesity, we investigated the effects of selective interference with CD28 signaling using knockout mice (Cd28KO) and a CTLA4-Ig fusion protein inhibiting CD28-B7 interactions.
resultsCd28 deficiency decreased pathogenic T cells and Treg content within AT without changing the macrophages number. Cd28KO epididymal but not subcutaneous fat was characterized by enlarged adipocytes, reduced levels of inflammatory cytokines and increased Glut4, adiponectin and lipogenic enzyme mRNA levels. This was associated with reduced inflammation, fat accumulation and enhanced glucose metabolism in liver. Weight gain and fasting glucose tolerance were not affected. CTLA4-Ig injections reduced the number of T cells in epididymal AT (epiAT) but not the inflammatory cytokines levels and failed to improve liver fat accumulation.
conclusionsDeletion of CD28 creates a new pro/anti-inflammatory balance in epiAT and liver and exerts a protective effect against hepatic steatosis.
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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.