Abstract
Since the late 1970s, the prevalence of allergic disease has increased substantially in industrialized countries where it has been linked to: increased hygiene and cleanliness;1 increased diesel pollution;2 increased use of carpets in which house dust mites grow;3 and decreased early childhood infections.4 During the early phases of allergic sensitisation, CD4 T helper cells become polarized to a T helper 2 (Th2) phenotype that is characterized by the cytokines interleukin (IL)-4, IL-5, IL-6, IL-9, IL-1 and IL-13.5–8 These Th2 cells provide help to B cells for class switching to immunoglobulin E (IgE)9,10 and contribute to the lung inflammation that causes asthma.11 Treatment of Th2-mediated immune diseases, to date, has focused on anti-inflammatory drugs and allergen immunotherapy with incremental doses of allergen. The latter is not completely understood but is associated with the induction of immunoglobulin G4 (IgG4) antibodies, increased T helper 1 (Th1) cytokines,12,13 as well as IL-10-producing regulatory T cells.14 In this issue of Immunology, Kim and colleagues15 show that Th2 immune responses can be redirected to Th1 by using anti-CD3 single-chain Fv/IL-18 fusion DNA.15
Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
