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Table 2 Human studies of IL-33 in allergic diseases

From: Biological mechanisms and therapeutic prospects of interleukin-33 in pathogenesis and treatment of allergic disease

Model of study

Result

Ref

placebo-controlled phase 2a study, for Etokimab(an anti–IL-33 biologic) to desensitize peanut-allergic adults(ClinicalTrials.gov NCT02920021)

- Reduce atopy-related adverse events

- Reduced IL-4, IL-5, IL-9, IL-13, ST2 levels

- Reduced peanut-specific IgE

[123]

Role of IL-33 and ST2R in human asthma patients

- Increased serum levels of soluble ST2

[17, 164]

Evaluate serum IL-33 in patients with asthma.

-Higher level of IL-33 in patients with asthma

-Higher IL-33 in the allergic asthma

-Higher serum IL-33 level in eosinophilic asthma

-No difference in serum IL-33 level between different asthma severity groups

[165]

IL-33 polymorphisms with asthma (rs4742170 and rs7037276, and rs1342326)

- rs4742170 and rs7037276 are associated with intermediate-onset wheeze

- rs1342326 is associated with persistent wheeze

- rs928413 and rs1342326 are relevant to asthma

[68, 166]

SNP in IL-33, rs1888909, rs1041973 and rs873022 are associated with

-Decreased production of sST2 in atopic

-Increases asthma risk

-Associated with post-bronchiolitis asthma

[167, 168]

IL-33 in HDM induced AR

-Stimulated Th2 cells to produce IL-5

-Responsible for induction of local inflammation

-IL-33 is crucial in the pathogenesis of chronic rhinosinusitis, nasal polyps

[106, 169]

IL-33 in asthma

-Greater IL-33 mRNA expression in epithelial cells of airway biopsies

-High levels of sST2 and IL-33 in the plasma and sputum

[72, 77]

Etokimab, a humanized immunoglobulin subtype G1/κ monoclonal Ab

-Inhibits IL-33 activity

-Inhibition of IL-33/IL-12–induced IFN-γ release in whole blood

[170]

24 Japanese cedar (JC) pollinosis patients and 14 HDM-sensitized patients with AR

-IL-33 protein level is increased in sinus mucosa

-significant correlation with the total nasal symptom score

[171]