Journal
ALLERGY
Volume 64, Issue 12, Pages 1728-1736Publisher
WILEY
DOI: 10.1111/j.1398-9995.2009.02201.x
Keywords
asthma; eosinophils; IgE; inflammation; omalizumab
Categories
Funding
- Novartis Pharma AG
- MRC [G19/34] Funding Source: UKRI
- Medical Research Council [G19/34] Funding Source: researchfish
Ask authors/readers for more resources
Asthma is a chronic inflammatory disease of the airways in which immunoglobulin E (IgE) plays a key role by activating a variety of inflammatory cells through interactions with Fc epsilon RI and Fc epsilon RII receptors. The role of IgE in allergic inflammation provided the rationale for developing omalizumab, a humanized monoclonal anti-IgE antibody, for patients with moderate-to-severe or severe allergic asthma. The reductions in circulating levels of IgE resulting from omalizumab treatment leads to reductions in Fc epsilon RI expression on mast cells, basophils and dendritic cells. This combined effect results in attenuation of several markers of inflammation, including peripheral and bronchial tissue eosinophilia and levels of granulocyte macrophage colony stimulating factor, interleukin (IL)-2, IL-4, IL-5 and IL-13. By blocking IgE binding to its receptors and diminishing dendritic cell Fc epsilon RI receptor expression, omalizumab may also reduce allergen presentation to T cells and the production of Th2 cytokines. The anti-inflammatory effects of omalizumab may, therefore, explain the reductions in asthma exacerbations and symptoms seen in clinical trials in patients with moderate-to-severe or severe, persistent, inadequately controlled allergic asthma.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available