The emerging role of IL-23 in asthma and its clinical implications

Figures & data

Table 1. FDA-approved monoclonal antibody therapies targeting the IL-23/Th17 axis.

Monoclonal Antibody	Target	FDA-approved indications
Ustekinumab	IL-12 p40 subunit	plaque psoriasis, psoriatic arthritis, Crohn’s disease
Guselkumab	IL-23 p19 subunit	psoriatic arthritis, plaque psoriasis
Risankizumab	IL-23 p19 subunit	psoriatic arthritis, Crohn’s disease
Tildrakizumab	IL-23 p19 subunit	plaque psoriasis
Brodalumab	IL-17 receptor	plaque psoriasis
Ixekizumab	IL-17A	plaque psoriasis, psoriatic arthritis, ankylosing spondylitis, axial spondyloarthritis
Secukinumab	IL-17A	plaque psoriasis, psoriatic arthritis, ankylosing spondylitis

FDA, Food and Drug Administration; IL, interleukin

Figure 1. Mechanisms of IL-23 signaling and IL-23/Th-17 blockade on T-cell-mediated inflammation. This figure illustrates proposed mechanisms by which IL-23 amplifies Th2- and Th17-mediated inflammation. In response to antigen stimulation, antigen presenting cells such as dendritic cells secrete IL-23, which primarily acts on Th17 cells to potentiate Th17 cell proliferation and function, thereby enhancing neutrophilic inflammation. It may also act on airway epithelium to increase secretion of alarmins, IL-33 and TSLP, which act on ILC2s to amplify the Th2 response. This may provide a pathway by which IL-23 increases eosinophilic inflammation, which is seen both clinically and in animal models. Created with BioRender.com.