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We found that hyperglycemia-induced OXTR reporter suppression occurred among the −2000, −1600, −1400, −1200, −1100, −800, −400 and −200 deletion constructs (numbered according to Ensembl gene ID: OXTR-201 ENST00000316793.7
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Particular emphasis is placed on the DC–T cell axis as a critical site where multiple metabolic defects converge, destabilizing antigen presentation, co-stimulation and immunological synapse function
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