1. Omalizumab in children with uncontrolled allergic asthma: Review of clinical trial and real-world experience 
Bradley E. Chipps, MD, Bob Lanier, MD, Henry Milgrom, MD, Antoine Deschildre, MD, Gunilla Hedlin, MD, Stanley J. Szefler, MD, Meyer Kattan, MD, Farid Kianifard, PhD, Benjamin Ortiz, MD, Tmirah Haselkorn, PhD, Ahmar Iqbal, MD, Karin Rosén, MD, Benjamin Trzaskoma, MS, William W. Busse, MD 
Journal of Allergy and Clinical Immunology 
Volume 139, Issue 5, Pages (May 2017)
DOI: /j.jaci
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2. Fig 1
Potential immune-inflammatory and cellular interactions contributing to the pathogenesis of asthma phenotypes and the role of omalizumab.8,17-26 Asthma is a chronic inflammatory disorder of considerable heterogeneity in which many cells, cellular mediators, and genetic and environmental factors play a role. Initial exposure to allergen leads to polarization of a TH2-type immune response involving activation of allergen-specific TH2 cells and IgE synthesis (sensitization). Subsequent allergen exposures cause inflammatory cell recruitment, activation, and mediator release.17,18 Nonallergic stimuli and intracellular pathogens/microbial infections tend to be responsible for the generation of TH1-type immune inflammatory responses, the predominance of neutrophils (ie, neutrophilia rather than eosinophilia), and suppression of TH2 cell proliferation.17,18 Omalizumab blocks IgE-receptor binding on the surface of immune cells, such as mast cells, preventing subsequent activation and release of mediators leading to tissue remodeling, inflammatory cell recruitment, and TH2-type inflammation CCL, CC chemokine ligand; CXCL, CXC chemokine ligand; DUOX, dual oxidase; EPO, eosinophil peroxidase; iNOS, inducible nitric oxide synthase; MUC, mucin; NO, nitric oxide; OX40/L, CD134 ligand; PGD2, prostaglandin D2; Tc1, cytotoxic T-cell type 1; TSLP, thymic stromal lymphopoietin.
Reproduced with permission of the American Thoracic Society and the European Respiratory Society.8
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 The Authors Terms and Conditions

3. Fig 2
Seasonal variation in frequency of exacerbations, as observed in the ICATA study.45 Band width represents the 95% CI. ICATA, Inner-City Anti-IgE Therapy for Asthma.
Copyright © 2016 Massachusetts Medical Society.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 The Authors Terms and Conditions

4. Fig 3
Proportion of participants with 1 or more exacerbations during the fall-season outcome period in the PROSE study.25 Proportion of participants by treatment arm with 1 or more exacerbations in the placebo and omalizumab arms randomized at steps 2 to 5 (A), placebo and omalizumab arms randomized at step 5 (B), and placebo, omalizumab, and ICS boost arms randomized at steps 2 to 4 (C). Values at the top of each panel are odds ratios (95% CIs). All values are adjusted for site, dosing group, and treatment step. Error bars are SEs.
Reprinted Teach et al.25 Copyright 2016, with permission from Elsevier.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 The Authors Terms and Conditions

5. Fig 4
Proportion of participants with 1 or more exacerbations during the fall-season outcome period in the PROSE study stratified by exacerbation status during the run-in phase.25 A, Placebo and omalizumab arms randomized at steps 2 to 5. B, Placebo and omalizumab arms randomized at step 5. C, Placebo, omalizumab, and ICS boost arms randomized at steps 2 to 4. Stratification according to participants experiencing exacerbation or no exacerbation during the run-in period are shown in the upper and lower panels, respectively. Values at the top of each panel are odds ratios (95% CIs). All values are adjusted for site, dosing group, and treatment step. Error bars are SEs. Bars represent placebo- and omalizumab-treated patients at all assigned treatment steps in the study.
Reprinted from Teach et al.25 Copyright 2016, with permission from Elsevier.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 The Authors Terms and Conditions

6. Fig 5
Enhanced ex vivo IFN-α responses to rhinovirus in the omalizumab group and relationship to exacerbation rates in the PROSE study.25 A, Pre- and post-randomization, patients' PBMCs were incubated ex vivo with rhinovirus in the presence or absence of an IgE cross-linking antibody, and IFN-α levels were measured in culture supernatants. A 3.22-fold increase in IFN-α levels were observed in the omalizumab group versus placebo in the postrandomization phase (P = .03). B, Among omalizumab-treated patients, those with the greatest increase in ex vivo IFN-α levels in the presence of IgE cross-linking were less likely to have an asthma exacerbation during the study outcome period. Values at the top of each panel are odds ratios (95% CIs). Error bars are SEs. RV, Rhinovirus.
Reprinted from Teach et al.25 Copyright 2016, with permission from Elsevier.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2017 The Authors Terms and Conditions