1. The MALT1 locus and peanut avoidance in the risk for peanut allergy
Alexandra Winters, PhD, Henry T. Bahnson, MPH, Ingo Ruczinski, PhD, Meher P. Boorgula, MS, Claire Malley, MS, Ali R. Keramati, MD, Sameer Chavan, MS, David Larson, PhD, Karen Cerosaletti, PhD, Peter H. Sayre, MD, PhD, Marshall Plaut, MD, George Du Toit, MB, BCh, FRCPCH, Gideon Lack, MB, BCh, FRCPCH, Kathleen C. Barnes, PhD, Gerald T. Nepom, MD, PhD, Rasika A. Mathias, ScD 
Journal of Allergy and Clinical Immunology 
Volume 143, Issue 6, Pages (June 2019)
DOI: /j.jaci
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2. Fig 1
Genome-wide association with peanut allergy at 60 months in 275 LEAP study participants in the peanut avoidance group. A, Genome-wide Manhattan plot for 4,444,069 SNVs with MAFs of 2% or greater, missingness of less than 5%, and Hardy-Weinberg equilibrium P values of 10−6 or greater. B, Quantile-quantile plot of the same data as in Fig 1, A. C, Peak association region on chromosome 18.
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3. Fig 2
A, Proportion of allergic and nonallergic LEAP study participants at 60 months of age by treatment group and MALT1 carrier status in all LEAP study participants (left) and the sensitized group (right; defined as those with peanut-specific IgE levels of 0.1 kU/L or greater at 60 months). B, IgE response to Ara h 1, Ara h 2, and Ara h 3 over the course of the LEAP study in all participants (n = 542). Arachis hypogaea status was imputed to 0 for all participants with peanut-specific IgE levels of less than 0.1 kU/L. C, Proportion of density plots showing relative distribution of peanut-specific IgE and IgE to Ara h 1, Ara h 2, and Ara h 3 between the MALT1 carrier and noncarrier groups at 60 months of age. The horizontal reference line at 12% indicates the proportion of the population with at least 1 MALT1 risk allele, which shows a null distribution with equal proportions of participants at all titer levels between the carriers and noncarriers. A hypogaea status was imputed to −2 (log10) for all participants with peanut-specific IgE levels of less than 0.1 kU/L. For all panels, imputed genotypes were used for 7 participants missing allele calls at rs , and noncarriers were defined as having at least 1 copy of the T allele (because of the low MAF; see Table E2 in this article's Online Repository at
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4. Fig E1
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5. Fig E2
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6. Fig E3
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7. Fig E4
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8. Fig E5
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9. Fig E6
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10. Fig E7
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11. Fig E8
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