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Interleukin (IL)-33 Immunobiology in Asthma and Airway Inflammatory Diseases

Supporting Files
File Language:
English


Details

  • Alternative Title:
    J Asthma
  • Personal Author:
  • Description:
    Objective:

    Identify key features of IL-33 immunobiology important in allergic and nonallergic airway inflammatory diseases and potential therapeutic strategies to reduce disease burden.

    Data Sources:

    PubMed, clinicaltrials.gov

    Study Selections:

    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.

    Results:

    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.

    Conclusion:

    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.

  • Keywords:
  • Source:
    J Asthma. 59(12):2530-2538
  • Pubmed ID:
    34928757
  • Pubmed Central ID:
    PMC9234100
  • Document Type:
  • Funding:
  • Volume:
    59
  • Issue:
    12
  • Collection(s):
  • Main Document Checksum:
    urn:sha256:714e428c3ea235a6aeec27a2c7173cf7ff15010ee0afd682b4723097452294da
  • Download URL:
  • File Type:
    Filetype[PDF - 466.86 KB ]
File Language:
English
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