Adult T‐cell Leukaemia in Patients With Okt4 Epitope Deficiency

Uozumi, Kimiharu; Ohno, Nobuhito; Ishizuka, Kenji; Iwahashi, M; Hanada, Shuichi; Arima, Terukatsu

doi:10.1111/j.1365-2141.1991.tb08098.x

Cited by 3 publications

(3 citation statements)

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“…The male ZDF rat displays a phenotype of progressive hyperglycaemia, reaching a state of overt diabetes that can be accelerated or intensified with HFD intake 177,178 . Apart from the expenses, the main drawback of this widespread model is the monogenic feature related to the mutation of the leptin receptor, which is uncommon in humans, thereby reducing the translational relevance 179 . Although some studies have shown typical features of overt diabetes in rat models of diet‐induced T2DM, particularly with long‐term protocols, the issue remains controversial, as diverse results have been reported.…”

Section: Diet‐induced Rodent Modelsmentioning

confidence: 99%

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Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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Diet is a critical element determining human health and diseases, and unbalanced food habits are major risk factors for the development of obesity and related metabolic disorders. Despite technological and pharmacological advances, as well as intensification of awareness campaigns, the prevalence of metabolic disorders worldwide is still increasing. Thus, novel therapeutic approaches with increased efficacy are urgently required, which often depends on cellular and molecular investigations using robust animal models. In the absence of perfect rodent models, those induced by excessive consumption of fat and sugars better replicate the key aspects that are the root causes of human metabolic diseases. However, the results obtained using these models cannot be directly compared, particularly because of the use of different dietary protocols, and animal species and strains, among other confounding factors. This review article revisits diet-induced models of obesity and related metabolic disorders, namely, metabolic syndrome, prediabetes, diabetes and nonalcoholic fatty liver disease. A critical analysis focused on the main pathophysiological features of rodent models, as opposed to the criteria defined for humans, is provided as a practical guide with a translational perspective for the establishment of animal models of obesity-related metabolic diseases.

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Section: Diet‐induced Rodent Modelsmentioning

confidence: 99%

“…relevance 179. Although some studies have shown typical features of overt diabetes in rat models of diet-induced T2DM, particularly with long-term protocols, the issue remains controversial, as diverse results have been reported.…”

mentioning

confidence: 99%

Diet‐induced rodent models of obesity‐related metabolic disorders—A guide to a translational perspective

et al. 2020

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“…It has been reported that about 8.3% of black Americans, 0.47% of Japanese, and 4.3% of black South African children are OKT4 epitope deficient 6–8 . Although OKT4 epitope deficiency has no effect on HIV‐1 infection and there is no evidence showing a direct relationship between OKT4 epitope deficiency and disease, this deficiency has been found in patients suffering systemic lupus erythematosus, acute myeloid leukemia, adult T‐cell leukemia, primary Sjogren's syndrome, psoriasis vulgaris, autoimmune thyroid disease, immunodeficiency, and human herpes virus 7 infection 9–15 . Here, we provide the first report on a case of OKT4 deficiency in a Chinese rhesus macaque (ChRM, Macaca mulatta ) and reveal that OKT4 epitope deficiency is a very old phenotype and may be parentally inherited.…”

Section: Introductionmentioning

confidence: 99%

Inherited OKT4 epitope deficiency in a Chinese rhesus macaque

Liu

Zhao

Wang

et al. 2021

J of Medical Primatology

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OKT4 is an important epitope of the CD4 molecular. Amino acid mutations in the CD4V3 region result in deficiency of the OKT4 epitope in human. Here, we firstly reported a case of hereditary deficiency of OKT4 epitope in an inbred Chinese rhesus macaque family. This epitope deficiency is due to cytosine to thymine transition and homozygote at the nucleotide position 793 of CD4 coding sequences, which leads to the replace of arginine at 265th position of CD4 molecule by tryptophan. The results reveal that OKT4 epitope deficiency is a very old phenotype and may be parentally inherited, and emphasize the importance of avoiding inbreeding in primate population breeding.

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