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Regulation of IgE homeostasis, and the identification of potential targets for therapeutic intervention
Uppsala University, Disciplinary Domain of Science and Technology, Biology, Department of Cell and Molecular Biology.
2007 (English)In: Biomedicine and Pharmacotherapy, ISSN 0753-3322, E-ISSN 1950-6007, Vol. 61, no 1, 34-49 p.Article, review/survey (Refereed) Published
Abstract [en]

Atopic allergies have increased during the past 20-30 years in frequency quite dramatically and in many countries have reached almost epidemic proportions. Allergies have thereby become one of the major medical issues of the western world. Inummoglobulin E (IgE) is here a central player. IgE is the Ig class that is present in the lowest concentration in human plasma. IgG is, for example, 10000 to 1 million times more abundant than IgE. However, despite of its low plasma levels IgE is a very important inducer of inflammation, due to its interaction with high-affinity receptors on mast cell and basophils. IgE has been conserved as a single active gene in all placental mammals studied, and the expression of this gene is under a very stringent control, most likely due to its very potent inflammatory characteristics. IgE expression is being regulated at many levels: by cytokines, switch region length, positive and negatively acting transcription factors and suppressors of cytokine signaling (SOCS). In addition, the plasma half-life differs markedly for IgG and IgE, with 21 and 2.5 days, respectively. This review summarizes the rapid progress in our understanding of the complex network of regulatory mechanisms acting on IgE and also how this new information may help us in our efforts to control IgE-mediated inflammatory conditions.

Place, publisher, year, edition, pages
2007. Vol. 61, no 1, 34-49 p.
Keyword [en]
IgE, mast cell, atopic allergies, isotype switch, cytokines
National Category
Immunology Immunology in the medical area
Identifiers
URN: urn:nbn:se:uu:diva-24331DOI: 10.1016/j.biopha.2006.10.001ISI: 000244918900005OAI: oai:DiVA.org:uu-24331DiVA: diva2:52105
Available from: 2007-02-05 Created: 2007-02-05 Last updated: 2017-12-07Bibliographically approved

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Hellman, Lars

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