> top > projects > Inflammaging > docs > PubMed:9108409 > annotations
Inflammaging  

PubMed:9108409 JSONTXT 10 Projects

Annnotations TAB TSV DIC JSON TextAE Lectin_function IAV-Glycan

Id Subject Object Predicate Lexical cue
T1 0-124 Sentence denotes Two distinct pathways of interleukin-5 synthesis in allergen-specific human T-cell clones are suppressed by glucocorticoids.
T1 0-124 Sentence denotes Two distinct pathways of interleukin-5 synthesis in allergen-specific human T-cell clones are suppressed by glucocorticoids.
T2 125-307 Sentence denotes Glucocorticoids (GC) have long been used as the most effective agents for the treatment of allergic diseases accompanied by eosinophilia such as chronic asthma and atopic dermatitis.
T2 125-307 Sentence denotes Glucocorticoids (GC) have long been used as the most effective agents for the treatment of allergic diseases accompanied by eosinophilia such as chronic asthma and atopic dermatitis.
T3 308-468 Sentence denotes The development of chronic eosinophilic inflammation is dependent on interleukin-5 (IL-5), a selective eosinophil-activating factor, produced by helper T cells.
T3 308-468 Sentence denotes The development of chronic eosinophilic inflammation is dependent on interleukin-5 (IL-5), a selective eosinophil-activating factor, produced by helper T cells.
T4 469-609 Sentence denotes To delineate the regulatory mechanisms of human IL-5 synthesis, we established allergen-specific CD4+ T-cell clones from asthmatic patients.
T4 469-609 Sentence denotes To delineate the regulatory mechanisms of human IL-5 synthesis, we established allergen-specific CD4+ T-cell clones from asthmatic patients.
T5 610-736 Sentence denotes GC efficiently suppressed IL-5 synthesis of T-cell clones activated via either T-cell receptor (TCR) or IL-2 receptor (IL-2R).
T5 610-736 Sentence denotes GC efficiently suppressed IL-5 synthesis of T-cell clones activated via either T-cell receptor (TCR) or IL-2 receptor (IL-2R).
T6 737-830 Sentence denotes Induction of IL-5 mRNA upon TCR and IL-2R stimulation was totally inhibited by dexamethasone.
T6 737-830 Sentence denotes Induction of IL-5 mRNA upon TCR and IL-2R stimulation was totally inhibited by dexamethasone.
T7 831-1205 Sentence denotes Human IL-5 promoter/enhancer-luciferase gene construct transfected to T-cell clones was transcribed on either TCR or IL-2R stimulation and was clearly downregulated by dexamethasone, indicating that the approximately 500-bp human IL-5 gene segment located 5' upstream of the coding region contains activation-inducible enhancer elements responsible for the regulation by GC.
T7 831-1205 Sentence denotes Human IL-5 promoter/enhancer-luciferase gene construct transfected to T-cell clones was transcribed on either TCR or IL-2R stimulation and was clearly downregulated by dexamethasone, indicating that the approximately 500-bp human IL-5 gene segment located 5' upstream of the coding region contains activation-inducible enhancer elements responsible for the regulation by GC.
T8 1206-1357 Sentence denotes Electrophoretic mobility shift assay analysis suggested that AP-1 and NF-kappaB are among the possible targets of GC actions on TCR-stimulated T cells.
T8 1206-1357 Sentence denotes Electrophoretic mobility shift assay analysis suggested that AP-1 and NF-kappaB are among the possible targets of GC actions on TCR-stimulated T cells.
T9 1358-1429 Sentence denotes NF-AT and NF-kappaB were not significantly induced by IL-2 stimulation.
T9 1358-1429 Sentence denotes NF-AT and NF-kappaB were not significantly induced by IL-2 stimulation.
T10 1430-1678 Sentence denotes Our results showing that GC suppressed IL-5 production by human CD4+ T cells activated by two distinct stimuli, TCR and IL-2R stimulation, underscore the efficacy of GC in the treatment of allergic diseases via suppression of T-cell IL-5 synthesis.
T10 1430-1678 Sentence denotes Our results showing that GC suppressed IL-5 production by human CD4+ T cells activated by two distinct stimuli, TCR and IL-2R stimulation, underscore the efficacy of GC in the treatment of allergic diseases via suppression of T-cell IL-5 synthesis.