1. Epigenome-wide analysis links SMAD3 methylation at birth to asthma in children of asthmatic mothers 
Avery DeVries, BS, Gabriela Wlasiuk, PhD, Susan J. Miller, MS, Anthony Bosco, PhD, Debra A. Stern, MS, I. Carla Lohman, MS, Janet Rothers, PhD, Anya C. Jones, PhD, Jessie Nicodemus-Johnson, PhD, Monica M. Vasquez, MPH, John A. Curtin, PhD, Angela Simpson, MD, PhD, Adnan Custovic, MD, PhD, Daniel J. Jackson, MD, James E. Gern, MD, Robert F. Lemanske, MD, Stefano Guerra, MD, Anne L. Wright, PhD, Carole Ober, PhD, Marilyn Halonen, PhD, Donata Vercelli, MD 
Journal of Allergy and Clinical Immunology 
Volume 140, Issue 2, Pages (August 2017)
DOI: /j.jaci
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2. Journal of Allergy and Clinical Immunology 2017 140, 534-542DOI: (10
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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3. Fig 1
Overview of study design. AA, Asthmatic child with an asthmatic mother; AN, asthmatic child with a nonasthmatic mother; NA, nonasthmatic child with an asthmatic mother; NN, nonasthmatic child with a nonasthmatic mother.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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4. Fig 2
Molecular interaction network of asthma-associated DMRs. The network was constructed by using all available interaction data in the Ingenuity Systems Knowledge Base. The most highly connected gene (SMAD3, 17 connections) is highlighted in black. Targets of IL1B, the top upstream regulator of network genes, are highlighted in gray. Types of interactive molecules are defined in the legend.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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5. Fig 3
Effects of maternal asthma on the association between neonatal SMAD3 methylation and childhood asthma in IIS (A), MAAS (B), and COAST (C). SMAD3 methylation in IIS and MAAS was assessed by means of bisulfite sequencing and expressed as a mean percentage of DNA methylation across 8 consecutive CpG sites in the SMAD3 DMR. In COAST percentage SMAD3 methylation at cg , the seventh CpG in the SMAD3 DMR, was assessed by using the Infinium HumanMethylation450 BeadChip array. A, Asthmatic; N, nonasthmatic. P values were determined by using the Wilcoxon 2-sample test. Results presented in Fig 3, A, were unaffected after adjusting for ethnicity.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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6. Fig 4
Effects of maternal asthma on the relation between neonatal SMAD3 methylation and IL-1β protein production. Distributions of SMAD3 methylation and log IL-1β–producing capacity in nonasthmatic and asthmatic children without and with a maternal history of asthma were compared by dividing mean percentage SMAD3 methylation and log IL-1β secretion at the median, thereby creating 4 groups (low/low, low/high, high/low, and high/high). Distributions for asthmatic and nonasthmatic subjects were compared across all 4 quadrants (A) or focusing the analysis on the high/high and low/low quadrants (B; P value determined with the Fisher exact test). A, Asthmatic; N, nonasthmatic.
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7. Fig E1
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8. Fig E2
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9. Fig E3
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10. Fig E4
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13. Fig E7
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14. Fig E8
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
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