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Immunopathogenesis of schistosomiasis
Thomas A Wynn1, Robert W Thompson, Allen W Cheever
1Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. twynn@niaid.nih.gov
Immunological Reviews
|September 14, 2004
Summary
Interleukin-13 (IL-13) drives schistosomiasis severity. Blocking IL-13 reduces liver fibrosis, while lacking the decoy receptor IL-13Ralpha2 worsens disease, highlighting its protective role.
Area of Science:
- Immunology
- Parasitology
- Pathology
Background:
- Schistosomiasis mansoni causes chronic inflammation, leading to liver scarring and portal hypertension.
- Tissue damage in schistosomiasis is linked to connective tissue deposition.
- Understanding disease severity mechanisms is crucial for schistosomiasis control.
Purpose of the Study:
- To elucidate the role of interleukin-13 (IL-13) in regulating schistosomiasis mansoni progression.
- To investigate the function of the IL-13 receptor complex in hepatic fibrogenesis and inflammation.
Main Methods:
- Utilized DNA microarrays and gene knock-out mouse models.
- Examined IL-13-deficient mice and IL-13 receptor alpha2 (IL-13Ralpha2)-deficient mice.
- Assessed liver fibrogenesis and granuloma formation in response to S. mansoni infection.
Main Results:
- IL-13 deficiency or antagonism significantly decreased liver fibrogenesis in infected mice.
- IL-13Ralpha2-deficient mice exhibited exacerbated hepatic fibrosis and inflammation.
- Lack of IL-13Ralpha2 impaired the downregulation of granuloma formation, leading to accelerated mortality.
Conclusions:
- Interleukin-13 (IL-13) is a central regulator of disease severity in schistosomiasis mansoni.
- The IL-13 receptor alpha2 (IL-13Ralpha2) acts as a critical 'off' switch, mitigating tissue-damaging inflammation.
- Targeting the IL-13 pathway, particularly IL-13Ralpha2, holds therapeutic potential for schistosomiasis.