Anti-interleukin 13 for asthma: stick or twist? Brian Lipworth, Sunny Jabbal, Chris RuiWen Kuo The Lancet Respiratory Medicine Volume 6, Issue 9, Pages e46-e47 (September 2018) DOI: 10.1016/S2213-2600(18)30275-3 Copyright © 2018 Elsevier Ltd Terms and Conditions
Figure 1 Diagram of biologics and biomarkers in relation to the type 2 inflammatory pathway in asthma Biologics (shown in light blue) include anti-IL-4Rα (dupilumab), anti-IL-5Rα (benralizumab), anti-IL-5 (mepolizumab or reslizumab), anti-IL-13 (tralokinumab or lebrikizumab), anti-IgE (omalizumab), and anti-TSLP (tezepelumab). Biomarkers include FENO, IgE, and eosinophils. IL-4=interleukin 4. IgE=immunoglobulin E. IL-4Rα=interleukin 4 receptor α. Th2=T-helper-2. IL-13=interleukin 13. FENO=fractional exhaled nitric oxide. TSLP=thymic stromal lymphopoietin. ILC-2=type 2 innate lymphoid cells. IL-5=interleukin 5. IL-5Rα=interleukin 5 receptor α. The Lancet Respiratory Medicine 2018 6, e46-e47DOI: (10.1016/S2213-2600(18)30275-3) Copyright © 2018 Elsevier Ltd Terms and Conditions
Figure 2 Blockade of IL-4 and IL-13 IL-13 and IL-4 are involved in trafficking eosinophils from blood vessels into the lungs. Blockade of IL-13 alone is insufficient to suppress tissue eosinophils in the presence of unopposed IL-4 signalling. Combined IL-4 and IL-13 blockade therefore results in putative reduction of lung eosinophils in conjunction with raised blood eosinophils. IL-13=interleukin 13. IL-4=interleukin 4. FENO=fractional exhaled nitric oxide. The Lancet Respiratory Medicine 2018 6, e46-e47DOI: (10.1016/S2213-2600(18)30275-3) Copyright © 2018 Elsevier Ltd Terms and Conditions