IL-24 promotes atopic dermatitis-like inflammation through driving MRSA-induced allergic responses.

Xinmin QIAN; Meiyi TONG; Tianqing ZHANG; Qingqing LI; Meng HUA; Nan ZHOU; Wenwen ZENG

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IL-24 promotes atopic dermatitis-like inflammation through driving MRSA-induced allergic responses.

Author: Xinmin QIAN ¹ ; Meiyi TONG ² ; Tianqing ZHANG ³ ; Qingqing LI ¹ ; Meng HUA ¹ ; Nan ZHOU ¹ ; Wenwen ZENG ¹
Author Information

1. Institute for Immunology and School of Basic Medical Sciences, Tsinghua Medicine, Tsinghua University, Beijing 100084, China.
2. Eight-year Medical Doctor Program, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing 100084, China.
3. School of Life Sciences, Tsinghua University, Beijing 100084, China.
Publication Type:Journal Article
Keywords: IL-24; MRSA; allergic inflammation; atopic dermatitis; keratinocytes
MeSH: Dermatitis, Atopic/genetics*; Interleukins/metabolism*; Animals; Methicillin-Resistant Staphylococcus aureus/immunology*; Mice; Keratinocytes/microbiology*; Humans; Interleukin-33/immunology*; Inflammation/microbiology*; Staphylococcal Infections/microbiology*; Disease Models, Animal; Hypersensitivity/microbiology*; Mice, Inbred C57BL
From: Protein & Cell 2025;16(3):188-210
CountryChina
Language:English
Abstract: Atopic dermatitis (AD) is a prevalent inflammatory skin disorder in which patients experience recurrent eczematous lesions and intense itching. The colonization of Staphylococcus aureus (S. aureus) is correlated with the severity of the disease, but its role in AD development remains elusive. Using single-cell RNA sequencing, we uncovered that keratinocytes activate a distinct immune response characterized by induction of Il24 when exposed to methicillin-resistant S. aureus (MRSA). Further experiments using animal models showed that the administration of recombinant IL-24 protein worsened AD-like pathology. Genetic ablation of Il24 or the receptor Il20rb in keratinocytes alleviated allergic inflammation and atopic march. Mechanistically, IL-24 acted through its heterodimeric receptors on keratinocytes and augmented the production of IL-33, which in turn aggravated type 2 immunity and AD-like skin conditions. Overall, these findings establish IL-24 as a critical factor for onset and progression of AD and a compelling therapeutic target.