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IL-33: a Janus cytokine.
1Institute of Infection, Immunity and Inflammation, University of Glasgow, 120, University Place, Glasgow G12 8TA, UK. foo.liew@glasgow.ac.uk
Annals of the Rheumatic Diseases
|March 31, 2012
Summary
Interleukin 33 (IL-33) enhances host defense against infections like Trichuris and sepsis. However, this immune mediator also exacerbates conditions such as allergies and arthritis, highlighting its dual role.
Area of Science:
- Immunology
- Molecular Biology
- Infectious Diseases
Background:
- Interleukin 33 (IL-33) is a cytokine belonging to the IL-1 family.
- IL-33 binds to the ST2 receptor, primarily found on Th2 cells and mast cells.
- IL-33 influences T-cell polarization, shifting from Th1 to Th2 phenotypes.
Purpose of the Study:
- To investigate the role of IL-33 in host defense mechanisms.
- To explore the impact of IL-33 on various inflammatory and infectious conditions.
- To evaluate the therapeutic potential and risks associated with IL-33 modulation.
Main Methods:
- Analysis of IL-33 gene expression during nematode infection (Trichuris muris).
- Assessment of IL-33 treatment effects on resistance to Trichuris infection.
- Evaluation of IL-33's role in sepsis models and atherosclerosis.
- Investigation of IL-33's influence on allergic responses and arthritis.
Main Results:
- IL-33 mRNA is upregulated early in Trichuris muris infection.
- IL-33 administration enhances resistance to Trichuris infection and attenuates sepsis.
- IL-33 reduces atherosclerosis and adipocyte inflammation by inducing type II cytokines.
- Conversely, IL-33 exacerbates allergic reactions and arthritis.
Conclusions:
- IL-33 plays a conserved role in host defense against infections.
- IL-33 exhibits context-dependent effects, acting as a double-edged sword.
- Targeting IL-33 requires careful consideration due to its potential to exacerbate certain inflammatory conditions.
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