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The Anti-IgE Therapy: From the Known and the Unknown

Arzu Didem Yalcin*

Internal Medicine, Allergy and Clinical Immunology, Academia Sinica, Genomics Research Center, Taiwan

*Corresponding author: Arzu Didem Yalcin MD. Internal Medicine, Allergy and Clinical Immunology, Academia Sinica, Genomics Research Center, 11529, Taipei, Taiwan, Tel: 8860278977509; E-mail:
Int J Aller Medcations; Volume 1, Issue 1 Editorial IJAM-1-001e
Received: February 10, 2015: Accepted: February 13, 2015: Published: February 16, 2015
Citation: Yalcin AD (2015) The Anti-IgE Therapy: From the Known and the Unknown. Int J Aller Medcations 1:001e
Copyright: © 2015 Yalcin AD. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Asthma is described as a complex disease arising from the contribution of multiple genetic and environmental factors [1,2]. Asthma is caused by multiple interacting genes, some having a protective effect and others contributing to the disease pathogenesis, with each gene having its own tendency to be influenced by the environment. At the end of 2010, 100 genes including IL-1R1,1RN, 3, 4, 5, 8RA, 9, 10, 12, 13, CTLA-4, and ADAM33, among others had been associated with asthma in six or more separate populations [3]. We have no idea about the effect of omalizumab on most of these genes. In our previous study we described that omalizumab reduces systemic inflammation such as oxidative stress markers and circulating apopitotic ligands. In an analysis of 8793 genes, sensitization of mast cells with monoclonal IgE alone, was found to upregulate 58 genes more than 2-fold compared with their levels in unsensitized mast cells. These genes included those for cytokines, and colony-stimulating factor 1; chemokines; and cytokine and chemokine receptors [4]. The mechanism of action of Omalizumab in the treatment of asthma or urticaria is believed to be multifactorial, and includes effects mediated through altered production of redox metabolites, and regulation of production of known inflammatory proteins.


We thank all participating patients and volunteers.

  1. Reddel HK, Taylor DR, Bateman ED, Boulet LP, Boushey HA, et al. (2009) An official American Thoracic Society/European Respiratory Society statement: asthma control and exacerbations: standardizing endpoints for clinical asthma trials and clinical practice. Am J Respir Crit Care Med 180: 59-99.

  2. Su MW, Tung KY, Liang PH, Tsai CH, Kuo NW, et al. (2012) Gene-gene and gene-environmental interactions of childhood asthma: a multifactor dimension reduction approach. PLoS One 7: e30694.

  3. Sandford A, Weir T, Paré P (1996) The genetics of asthma. Am J Respir Crit Care Med 153: 1749-1765.

  4. Yalcin AD (2015) Advances in Anti-IgE Therapy. Biomed Reseach International.

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