ArticleMedical science monitor : international medical journal of experimental and clinical research2018
Role of Natural Killer T (NKT) Cells in Type II Diabetes-Induced Vascular Injuries.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 26 citations in OpenAlex.
- Natural killer cell levels in adults living with type 2 diabetes: a systematic review and meta-analysis of clinical studies.BMC immunology · 2020Pooled it
- Article
- High glucose/ChREBP-induced Hif-1α transcriptional activation in CD4Diabetologia · 2025Article
- Metabolic and Immune Parameters in Pregnant Women with Impaired Glucose Metabolism-A Pilot Study.Metabolites · 2024Article
- Association of immune cell composition with the risk factors and incidence of acute coronary syndrome.Clinical epigenetics · 2023Article
- T cells and their products in diabetic kidney disease.Frontiers in immunology · 2023Review
- Dysfunction of circulating CD3International journal of medical sciences · 2023Article
- Urinary tract infection in patients with diabetes mellitus and the role of parental genetics in the emergence of the disease.Journal of medicine and life · 2022Article
- Raised SPINK1 levels play a role in angiogenesis and the transendothelial migration of ALL cells.Scientific reports · 2022Article
- Angiotensin-(1-7) ameliorates high glucose-induced vascular endothelial injury through suppressing chloride channel 3.Bioengineered · 2022Article
- Tim-3 Expression Causes NK Cell Dysfunction in Type 2 Diabetes Patients.Frontiers in immunology · 2022Article
- Diabetes mellitus exacerbates experimental autoimmune myasthenia gravis via modulating both adaptive and innate immunity.Journal of neuroinflammation · 2021Article
- T-Natural Killers and Interferon Gamma/Interleukin 4 in Augmentation of Infection in Foot Ulcer in Type 2 Diabetes.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Article
- The Effects of Type 2 Diabetes Mellitus on Organ Metabolism and the Immune System.Frontiers in immunology · 2020Review
- Role of inflammatory cells in pathophysiology and management of diabetic retinopathy.Survey of ophthalmologyReview
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND This study investigated the distribution and features of natural killer T (NKT) cells in the peripheral blood of diabetic patients, and their regulatory roles on vascular endothelial cells. MATERIAL AND METHODS Peripheral lymphocytes were isolated from diabetic patients. NKT cell distribution, proportion, and surface and intracellular markers were detected with flow cytometry. Peripheral blood-derived NKT cells were isolated and co-cultured with human umbilical vein endothelial cells (HUVECs). Proliferation and migration of HUVECs were assessed with the CCK-8 assay and the Transwell chamber assay. RESULTS The ratios of CD3-CD56+ NK and CD3+CD56+ NKT cells in the peripheral blood of patients with type II diabetes were significantly elevated. The expression levels of NKp30, NKG2D, and NKp44 on the surface were increased in the CD3+CD56+ NKT cells, while the expression levels of NKG2A and 158b were significantly downregulated. The expression level of granzymes in the peripheral blood-derived NKT cells were not changed in patients with type II diabetes, but the expression levels of IFNg and IL-4 were significantly increased. However, after co-culture with NKT cells derived from the peripheral blood of diabetic patients, the proliferation and migration of HUVECs were significantly inhibited, and was restored by treatment with IL-4 antibody. In addition, the IL-4 stimulus inhibited the proliferation and migration of HUVECs. ls were not changed in patients with type II diabetes, while the expression levels of IFNγ and IL-4 were significantly increased. However, after co-cultured with NKT cells derived from the peripheral blood of diabetic patients, the proliferation and migration of HUVECs were significantly inhibited, which could significantly restored by the treatment of IL-4 antibody. In addition, the IL-4 stimulus could down-regulate the proliferation and migration of HUVECs. CONCLUSIONS Peripheral blood NKT cells are increased and activated in diabetes. NKT cells inhibit the proliferation and migration of HUVECs by secreting IL-4, thereby inducing vascular injuries.
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