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

Author:

Qian Xinmin1ORCID,Tong Meiyi23ORCID,Zhang Tianqing3ORCID,Li Qingqing1ORCID,Hua Meng1,Zhou Nan1,Zeng Wenwen1456ORCID

Affiliation:

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

4. SXMU-Tsinghua Collaborative Innovation Center for Frontier Medicine, Shanxi Medical University , Taiyuan 030001 , China

5. Tsinghua-Peking Center for Life Sciences , Beijing 100084 , China

6. Beijing Key Laboratory for Immunological Research on Chronic Diseases , Beijing 100084 , China

Abstract

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.

Funder

National Key R&D Program of China

National Natural Science Foundation of China

Publisher

Oxford University Press (OUP)

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