1. Distinct transcriptome profiles differentiate nonsteroidal anti-inflammatory drug– dependent from nonsteroidal anti-inflammatory drug–independent food-induced anaphylaxis 
Rosa Muñoz-Cano, MD, PhD, Mariona Pascal, PhD, Joan Bartra, MD, PhD, Cesar Picado, MD, PhD, Antonio Valero, MD, PhD, Do-Kyun Kim, PhD, Stephen Brooks, PhD, Michael Ombrello, MD, Dean D. Metcalfe, MD, Juan Rivera, PhD, Ana Olivera, PhD 
Journal of Allergy and Clinical Immunology 
Volume 137, Issue 1, Pages (January 2016)
DOI: /j.jaci
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2. Fig 1
Increased ROS levels and the top-scored gene network in comparison of patients with NSAID-LTP-A and those with LTP-A. A, Serum levels of free radicals (ROS and reactive nitrogen species [RNS]) in the indicated groups. Data are expressed as means ± SEMs. **P < .01 and ***P < .001 compared with HVs. B, Functional relationships of differentially expressed genes in patients with NSAID-LTP-A versus those with LTP-A in the top-scored network: cell death and survival, inflammatory response, and cancer. The intensity of the node color indicates the degree of upregulation (red) or downregulation (green). Genes in uncolored nodes were of relevance for this network and integrated into the computationally generated networks on the basis of the evidence stored in the IPA knowledge memory, but they were not identified as differentially expressed. Lines indicate molecular interactions.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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3. Fig 2
LTP-specific IgG1/IgG3 in sera from patients with LTP-A and repressed IFN-γ and IFN-γ–regulated genes in patients with NSAID-LTP-A. A, Representation of IFNG as an upstream regulator of differentially regulated genes in patients with NSAID-LTP-A compared with those with LTP-A, as identified by using IPA. The arrows connect genes with altered expression that might be regulated by IFNG. The style of the lines defines the direction of change. The color of the node indicates the direction of gene regulation. Gray, Downregulated; blank, upregulated. B and C, Serum levels of IFN-γ (Fig 2, B) and IgG1 and IgG3 anti–Pru p 3 (Fig 2, C) in the indicated groups. Data are expressed as means ± SEMs. *P < .05, **P < .01, and ***P < .001 compared with HVs, unless otherwise indicated.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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4. Fig 3
Differentially expressed genes in patients with NSAID-LTP-A compared with those with LTP-A. Genes in gray boxes indicate their association with TH2-type of immunity, whereas genes in blue boxes indicate association with TH1-type immunity. Differences between groups were statistically significant (P < .05), unless otherwise indicated. NS, Not significant. Columns 3 to 5 were color coded in accordance with the fold change.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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5. Fig E1
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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6. Fig E2
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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