Marcia A Chan, Nicole M Gigliotti, Abby L Dotson and Lanny J Rosenwasser
For all author emails, please log on.
Clinical and Translational Allergy 2013, 3:29 doi:10.1186/2045-7022-3-29
Published: 2 September 2013Abstract (provisional)
Background
Omalizumab, is a humanized anti-IgE monoclonal antibody used to treat allergic asthma. Decreased serum IgE levels, lower eosinophil and B cell counts have been noted as a result of treatment. In vitro studies and animal models support the hypothesis that omalizumab inhibits IgE synthesis by B cells and causes elimination of IgE-expressing cells either by induction of apoptosis or induction of anergy or tolerance.
Methods
We examined the influence of omalizumab on human tonsillar B cell survival and on the genes involved in IgE synthesis. Tonsillar B cells were stimulated with IL-4 plus anti-CD40 antibody to induce class switch recombination to IgE production in the presence or absence of omalizumab. Cell viability was assessed and RNA extracted to examine specific genes involved in IgE synthesis.
Conclusions
We found that omalizumab reduced viable cell numbers but this was not through induction of apoptosis. IL-4R and germline Cepsilon mRNA levels were decreased as well as the number of membrane IgE+ cells in B cells treated with omalizumab. These data suggest that omalizumab may decrease IgE synthesis by human B cells by specifically targeting membrane IgE-bearing B cells and inducing a state of anergy.
The complete article is available as a provisional PDF. The fully formatted PDF and HTML versions are in production. |
No comments:
Post a Comment