The pathogenicity of IL-33 on steroid-resistant eosinophilic inflammation via the activation of memory-type ST2 + CD4 + T cells

Journal of Leukocyte Biology: An Official Publication of the Reticuloendothelial Society

article

Kiyoshi Hirahara¹  Naoko Mato³  Koichi Hagiwara³  Toshinori Nakayama¹ 

[1] Department of Immunology, Graduate School of Medicine, Chiba University;AMED-PRIME, AMED;Division of Pulmonary Medicine, Department of Internal Medicine, Jichi Medical University

关键词: eosinophilic pneumonia;    epithelial cytokine;    iBALT;    pathogenic Th2;   

DOI  :  10.1002/JLB.MR1117-456R

学科分类：生理学

来源: Federation of American Societies for Experimental Biology

【 摘 要 】

The lungs are the primary organs of the respiratory system in many animals and have unique epithelial barrier systems to protect the host from continuous invasion of various harmful particles, such as viruses and bacteria. IL-33, a member of the IL-1 family of cytokines, is released from epithelial cells in the mucosal organs and drives the type 2 immune response by activating a number of immune cells in cases of helminth infection. However, IL-33 derived from epithelial cells also causes various allergic diseases via the activation of ST2-positive immune cells, including memory-type (CD62LlowCD44hi) ST2+CD4+ T cells in the lung. Recent studies have revealed that the type 2 inflammation induced by IL-33 is steroid resistant. Steroid resistance causes severe chronic inflammatory diseases, such as intractable asthma. In this review, we will discuss the impact of ST2+CD4+ T cells on shaping the pathology of IL-33-induced eosinophilic inflammation. We will also highlight the mechanism underlying steroid resistance in eosinophilic pneumonia. A better understanding of the cellular and molecular mechanisms underlying steroid resistance is crucial for the development of new therapeutic strategies for intractable allergic diseases.

【 授权许可】

CC BY