INT226394

Context Info Confidence 0.05 First Reported 2008 Last Reported 2008 Negated 2 Speculated 0 Reported most in Body Documents 1 Total Number 2 Disease Relevance 0.97 Pain Relevance 0.28

cell differentiation (Hand2) nucleus (Hand2) DNA binding (Hand2) protein complex (Hand2) transcription factor binding (Hand2)

Anatomy Link Frequency dendritic cells 3 macrophages 1 Hand2 (Mus musculus)

Pain Link Frequency Relevance Heat cytokine 182 86.88 Inflammation 192 55.04 chemokine 46 47.28 antagonist 68 5.00 agonist 40 5.00 Inflammatory response 12 5.00 methotrexate 8 5.00 Inflammatory mediators 4 5.00 withdrawal 4 5.00 cINOD 4 5.00

Disease Link Frequency Relevance Heat Occupational Lung Diseases 30 91.76 Organ Transplantation 2 82.96 Asthma 630 73.16 INFLAMMATION 206 55.04 Apoptosis 18 34.92 Targeted Disruption 40 5.00 Eosinophilia 38 5.00 Disease 34 5.00 Rhinitis 22 5.00 Hypersensitivity 18 5.00

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Key:

Protein

Mutation

Event

Anatomy

Negation

Speculation

Pain term

Disease term

Glucocorticoids, in vitro (a) inhibit IL-12 secretion from monocyte-macrophages and dendritic cells, (b) decrease IL-12 receptor 1- and 2-chain expression, thereby inhibiting IL-12 signaling, and (c) inhibit IL-12-induced STAT-4 (transcription factor that drives Th1 differentiation) phosphorylation without affecting STAT-6 (transcription factor that drives Th2 differentiation) phosphorylation (d), and thereby deviate the immune response predominantly toward the Th2 phenotype [8,12].

Neg (without) Regulation (affecting) of Phosphorylation (phosphorylation) of Th2 in dendritic cells

1) Confidence 0.05 Published 2008 Journal J Occup Med Toxicol Section Body Doc Link PMC2259400 Disease Relevance 0.49 Pain Relevance 0.14

Glucocorticoids, in vitro (a) inhibit IL-12 secretion from monocyte-macrophages and dendritic cells, (b) decrease IL-12 receptor 1- and 2-chain expression, thereby inhibiting IL-12 signaling, and (c) inhibit IL-12-induced STAT-4 (transcription factor that drives Th1 differentiation) phosphorylation without affecting STAT-6 (transcription factor that drives Th2 differentiation) phosphorylation (d), and thereby deviate the immune response predominantly toward the Th2 phenotype [8,12].

Neg (without) Regulation (affecting) of in macrophages Phosphorylation (phosphorylation) of Th2 in dendritic cells

2) Confidence 0.02 Published 2008 Journal J Occup Med Toxicol Section Body Doc Link PMC2259400 Disease Relevance 0.49 Pain Relevance 0.14

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