Immunomodulatory effects of IL‐23 and IL‐17 in a mouse model of allergic rhinitis

Abstract

IL-17 and IL-23 may play a pathogenic role in an established AR mouse model; with a more pronounced contribution of IL-23 than IL-17.

IL-23, rather than IL-17, is crucial for the development of ovalbumin-induced allergic rhinitis

“…Anti-IL-23 Ab treatment significantly alleviated nasal symptoms, accompanied by reduced Th2 responses, serum OVA-specific IgE, as well as nasal neutrophil, eosinophil and mast cell infiltration (Wang et al, 2013). In this study, we found that the mRNA levels of IL-23 and IL-17 in the nasal mucosa were significantly increased in OVA-treated mice.…”

“…However, we found that neither IL-23 nor IL-17 was necessary for sub-mucosal thickening during chronic AR induced by OVA. Furthermore, IL-23 was reportedly produced/expressed by various types of immune cells (such as macrophages, dendritic cells and mast cells) as well as non-immune cells (such as epithelial cells, endothelial cells and fibroblasts) (Sherlock et al, 2015;Wang et al, 2013). Our findings suggest that immune-cellderived IL-23 is not essential for development of OVA-induced AR.…”

“…Wang et al (2013) reported that IL-17 has a pathogenic role in this wellestablished mouse model of AR, and its effects are limited to the Th2 responses, nasal neutrophil and eosinophil infiltration. A previous study demonstrated that the failure of anti-IL-17Ab to inhibit OVA-specific Ig-E and mast cell infiltration may contribute to its failure to alleviate nasal symptoms, because IgE levels are related to mast cell migration and activation (Mathias et al, 2009).…”

Inflammatory cytokines in pediatric obstructive sleep apnea

“…[28] IL-23 is a cytokine with immunomodulatory effects. [29] It acts on memory-cluster-designation-4 (+) T cells, activates the transcription activator, and stimulates the production of interferon-gamma. [30,31] Studies showed that TH17 cells can be regulated by IL-23.…”

Pivotal role of cerebral interleukin-23 during immunologic injury in delayed cerebral ischemia in mice

“…Significantly increased IL-23p19 expression, both at messenger ribonucleic acid (mRNA) and protein levels, was demonstrated in multiple sclerotic lesions (Li http et al, 2007). Meanwhile, anti-IL-23p19 antibody is effective in treating certain autoimmune diseases (Elson et al, 2007;Cornelissen et al, 2013;Wang et al, 2013). Thus, from a therapeutic viewpoint, IL-23p19 might represent a new target for ischemic stroke therapy.…”