Interleukin (IL)-33 immunobiology in asthma and airway inflammatory diseases.
Interleukin (IL)-33 immunobiology in asthma and airway inflammatory diseases.
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DOI:
10.1080/02770903.2021.2020815
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发表时间:
2022-12
期刊:
影响因子:
--
通讯作者:
中科院分区:
文献类型:
--
作者:
Identify key features of IL-33 immunobiology important in allergic and nonallergic airway inflammatory diseases and potential therapeutic strategies to reduce disease burden. PubMed, clinicaltrials.gov A systematic and focused literature search was conducted of PubMed from March 2021 to December 2021 using keywords to either PubMed or BioMed Explorer including IL-33/ST2, genetic polymorphisms, transcription, translation, post-translation modification, nuclear protein, allergy, asthma, and lung disease. Clinical trial information on IL-33 was extracted from clinicaltrials.gov in August 2021. In total, 72 publications with relevance to IL-33 immunobiology and/or clinical lung disease were identified (allergic airway inflammation/allergic asthma n = 26, non-allergic airway inflammation n = 9, COPD n = 8, lung fibrosis n = 10). IL-33 levels were higher in serum, BALF and/or lungs across inflammatory lung diseases. Eight studies described viral infections and IL-33 and 4 studies related to COVID-19. Mechanistic studies (n = 39) including transcript variants and post-translational modifications related to the immunobiology of IL-33. Single nucleotide polymorphism in IL-33 or ST2 were described in 9 studies (asthma n = 5, inflammatory bowel disease n = 1, mycosis fungoides n = 1, ankylosing spondylitis n = 1, coronary artery disease n = 1). Clinicaltrials.gov search yielded 84 studies of which 17 were related to therapeutic or biomarker relevance in lung disease. An integral role of IL-33 in the pathogenesis of allergic and nonallergic airway inflammatory disease is evident with several emerging clinical trials investigating therapeutic approaches. Current data support a critical role of IL-33 in damage signaling, repair and regeneration of lungs.
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DOI:
10.2147/dmso.s251978
发表时间:
2020
期刊:
Diabetes, metabolic syndrome and obesity : targets and therapy
影响因子:
--
作者:
Hasan A;Kochumon S;Al-Ozairi E;Tuomilehto J;Al-Mulla F;Ahmad R
通讯作者:
Ahmad R
影响因子:
4.6
作者:
Gatti F;Mia S;Hammarström C;Frerker N;Fosby B;Wang J;Pietka W;Sundnes O;Hol J;Kasprzycka M;Haraldsen G
通讯作者:
Haraldsen G
影响因子:
2.7
作者:
Hayakawa H;Hayakawa M;Tominaga SI
通讯作者:
Tominaga SI
影响因子:
24.1
作者:
通讯作者:
--
影响因子:
4.4
作者:
Fu, Zhirong;Thorpe, Michael;Hellman, Lars
通讯作者:
Hellman, Lars