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Researchers Distinguish IL-24 as Pivotal Mediator of Pro-inflammatory, Allergic Skin Diseases

Article

Researchers exhibit recent advances in the basic characteristics of interleukin (IL)-24, a member of the IL-20 family of cytokines associated with pro-inflammatory autoimmune disorders such as psoriasis, arthritis, and inflammatory bowel diseases, as a catalyst in the pathogenesis of allergic skin inflammation.

In addition to research linking interleukin (IL)-24 as a catalyst of pro-inflammatory autoimmune disorders such as psoriasis, arthritis, and inflammatory bowel diseases, researchers distinguish the gene’s role in the pathogenesis of allergic skin inflammation in a recent article.

Published in the journal Allergology International, researchers developed a review of the IL-24 gene, a member of the IL-20 family of cytokines produced by various types of cells, including keratinocytes, bronchial epithelial cells, and myofibroblasts. IL-24 has been linked in previous studies as an essential figure in the pathogenesis of pro-inflammatory autoimmune disorders such as psoriasis, arthritis, and inflammatory bowel diseases, but as study authors note, “the role of IL-24 in the pathogenesis of allergic diseases has been elusive.”

Prior research on IL-24 in association to allergic diseases has shown its involvement in the pathogenesis of allergic lung and skin diseases, with further relationships found recently by study authors linking the gene to IL-13—mediated skin barrier dysfunction in atopic dermatitis (AD). In the review, researchers show recent advances in the basic characteristics of IL-24 and its novel functions in the pathogenesis of allergic skin inflammation, focusing on AD.

Pathogenic Role of IL-24 in Pro-Inflammatory Autoimmune Diseases, Allergic Disorders

Researchers highlight that the binding of IL-20 receptors with IL-24 has been reported to activate Janus kinases and subsequently signal transducer and activator of transcription (STAT) 3. STAT3 is known to be overexpressed and activated in psoriatic skin, with further expression of constitutively active STAT3 in epidermal keratinocytes shown to cause psoriasis-like skin inflammation in mice. “Similarly, keratinocytes from psoriasis patients show higher expression of IL-24 than those from control patients,” said the study authors.

In an analysis conducted by the study authors, IL-24 was discovered to have crucial roles in barrier dysfunction and S. aureus infection. Similarly, in AD, a skin disorder characterized by IgE elevation and skin barrier dysfunction, patients show abnormal skin barriers that are frequently colonized with S. aureus. As IL-24’s relation with STAT3 is known to cause psoriatic inflammation, study authors note the significance of IL-24 as a mediator for the development of AD.

Researchers note that as the role of IL-24 in allergic diseases is still not fully understood, further research is needed to improve knowledge of this association. “A better understanding of the role of IL24 in allergic diseases can lead to the development of new therapeutic options,” said the study authors.

Reference

Mitamura Y, Nunomura S, Furue M, et al. IL-24: A new player in the pathogenesis of pro-inflammatory and allergic skin diseases [published online January 21, 2020]. Allergol Int. doi: 10.1016/j.alit.2019.12.003.

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