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(2018). https://pubmed.ncbi.nlm.nih.gov/29531163/ DOI: 10.4049/jimmunol.1701200","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Activated CD4 T cells","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"nutrient_deficiency","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"5e4f0373-efbd-5f75-a096-27cf9eb9683d","evidence_kind":"source_excerpt","locator":"Lines 1066-1077","start_line":1066,"end_line":1077,"excerpt":"### b7-immune-tnf\nBiotin-deficient human CD4 T cells secreted more TNF after anti-CD3/CD28 stimulation.\nCondition category: nutrient_deficiency\nnutrient_topic: Biotin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A second inflammatory signal also increased.\norganism: Homo sapiens\ntissue_or_cell_type: Activated CD4 T cells\nexperimental_model: Anti-CD3/CD28-stimulated human CD4 T cells in biotin-deficient culture; separate mouse validation\nlimitations: Cell-culture inflammation does not show that extra biotin treats autoimmune disease in replete people.\nexposure: Defined biotin deficiency and signaling experiments\nevidence_span: {\"source_cache\": \"artifacts/biotin-research/29531163.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f\", \"start_char\": 0, \"end_char\": 1720, \"text_sha256\": \"64511b88fc7991ad24a1d7c122f5147b1bd99522532fa61752b439f39d363b6f\"}\n[b7-p29531163] Biotin Deficiency Induces Th1- and Th17-Mediated Proinflammatory Responses in Human CD4+ T Lymphocytes via Activation of the mTOR Signaling Pathway. 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