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Critical Reviews™ in Immunology
インパクトファクター: 1.352 5年インパクトファクター: 3.347 SJR: 0.657 SNIP: 0.55 CiteScore™: 2.19

ISSN 印刷: 1040-8401
ISSN オンライン: 2162-6472

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Critical Reviews™ in Immunology

DOI: 10.1615/CritRevImmunol.2016015865
pages 451-461

Interleukin-33 and its Receptor in Pulmonary Inflammatory Diseases

Jing Zhao
Department of Medicine, University of Pittsburgh School of Medicine, Acute Lung Injury Center of Excellence, and Vascular Medical Institute, University of Pittsburgh, Pittsburgh, PA, United States
Yutong Zhao
Department of Medicine, University of Pittsburgh School of Medicine, Acute Lung Injury Center of Excellence, and Vascular Medical Institute, University of Pittsburgh, Pittsburgh, PA, United States

要約

Interleukin-33 (IL-33) is a member of the IL-1 cytokine family. It modulates immune responses and biological functions through binding to its membrane receptor, ST2L. ST2L is a member of the Toll-like/IL-1 (TIR)-receptor superfamily, and its isoform, soluble ST2 (sST2), functions as an inhibitor of the IL-33/ST2L pathway. Levels of IL-33 and sST2 in serum and bronchoalveolar lavage fluid (BAL) are known biomarkers for a variety of disorders such as heart failure, non-small-cell lung cancer, and pulmonary inflammatory diseases. IL-33 also exists in the nuclei, and nuclear IL-33 seems to regulate cytokine gene expression. In this review, we focus on the role of IL-33/ST2 in the pathogenesis of pulmonary inflammatory diseases including asthma, chronic obstructive pulmonary disease (COPD), and lung injury.