1. IL-13 in asthma and allergic disease: Asthma phenotypes and targeted therapies 
Jennifer L. Ingram, PhD, Monica Kraft, MD 
Journal of Allergy and Clinical Immunology 
Volume 130, Issue 4, Pages (October 2012)
DOI: /j.jaci
Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

2. Fig 1
Overview of the cellular effects of IL-13 on airway inflammatory and structural cells in asthmatic patients. Mast cells, TH2 cells, and innate lymphoid cells secrete IL-13 on inhaled allergen stimulation. IL-13 triggers macrophage and eosinophil activation to accelerate airway inflammation, IgE production by B cells, smooth muscle cell activation contributing to airways hyperresponsiveness, mucus and growth factor production in airway epithelial cells, eotaxin production to stimulate eosinophil recruitment to the airway, and activation/proliferation/migration of airway fibroblasts to promote airway remodeling. Adapted from Kraft.6 AAM, Alternatively activated macrophage; iNOS, inducible nitric oxide synthase; MCP-1, monocyte chemoattractant protein; PGD2, prostaglandin D2; SCF, stem cell factor; Treg, regulatory T; TSLP, thymic stromal lymphopoietin.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

3. Fig 2
Schematic representation of the IL-4/IL-13 receptors and signaling pathways. IL-4 binds to either the type I receptor, which is composed of the IL-4Rα and common γ chain heterodimer, or to the type II receptor, which is composed of the IL-4Rα and IL-13Rα1 heterodimer. IL-13 binds to either the IL-13Rα1 subunit or to the high-affinity IL-13Rα2 subunit. IL-13Rα2 has been hypothesized to act as a decoy receptor, but reports of signaling by IL-13Rα2 have challenged this notion. IL-13/IL-4–induced gene expression is mediated predominantly through a phosphorylation cascade initiated on IL-4Rα with signaling through the Janus kinase (JAK)/STAT6 pathway.
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions

4. Fig 3
Serum periostin levels inform efficacy of anti–IL-13 therapy to treat airway obstruction. In a study by Corren et al,106 patients were stratified before treatment with lebrikizumab by using baseline serum periostin levels. After 12 weeks of treatment with the antibody, the increase in FEV1 was higher in the lebrikizumab group compared with that seen in the placebo group (A), but an even greater increase in FEV1 with lebrikizumab was observed in the high-periostin subset of patients (B). In the low-periostin subgroup the change in FEV1 was not significant (C).
Excerpted from Corren et al.106
Journal of Allergy and Clinical Immunology  , DOI: ( /j.jaci )
Copyright © 2012 American Academy of Allergy, Asthma & Immunology Terms and Conditions