Skip to main content
padlock icon - secure page this page is secure

Free Content EBI3 deficiency leads to diminished T helper type 1 and increased T helper type 2 mediated airway inflammation

Download Article:

Despite extensive investigation of the signals required for development of T helper type 1 (Th1) and type 2 (Th2) immune responses, the mechanisms involved are still not well-defined. A critical role for Epstein–Barr virus-induced gene 3 (EBI3) in these responses has been proposed. EBI3, initially discovered as a transcriptionally activated gene in Epstein–Barr virus-infected B lymphocytes, codes for a subunit of the cytokine interleukin-27 (IL-27). While initial studies suggested that it had an important role in promoting Th1 responses, subsequent studies have revealed that EBI3 receptor signalling influences a variety of immune cell types and can inhibit both Th1 and Th2 responses. In the present study, we evaluated EBI3−/− mice for their ability to mount both Th1-mediated and Th2-mediated airway inflammatory responses. The EBI3−/− mice sensitized by exposure to inhaled ovalbumin plus a high dose of lipopolysaccharide, which normally results in Th1 responses in wild-type (WT) mice, instead developed Th2 type airway inflammation, with increased numbers of eosinophils. The EBI3−/− mice that were exposed to inhaled ovalbumin with a low dose of lipopolysaccharide, which induces Th2 responses in WT mice, showed a marked enhancement of these responses, with increased airway eosinophils, increased serum IgE levels and increased levels of Th2 cytokines (IL-4, IL-5 and IL-13) in culture supernatants of mediastinal lymph node cells. Increased production of Th2 cytokines was also seen when naive CD4+ T cells from EBI3−/− mice were stimulated in vitro compared with cells from WT mice. These results provide the first evidence that EBI3 may play an inhibitory role in allergic asthma development.
No References
No Citations
No Supplementary Data
No Article Media
No Metrics

Keywords: CD4/helper T cells; EBI3; allergic asthma; cytokines; mice

Document Type: Research Article

Affiliations: 1: Department of Pediatrics, Section of Pediatric Pulmonology, Yale University School of Medicine, New Haven, CT 2: Department of Dermatology, Yale University School of Medicine, New Haven, CT 3: President’s Office, Wellesley College, Wellesley, MA, USA

Publication date: April 1, 2011

  • Access Key
  • Free content
  • Partial Free content
  • New content
  • Open access content
  • Partial Open access content
  • Subscribed content
  • Partial Subscribed content
  • Free trial content
Cookie Policy
Cookie Policy
Ingenta Connect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more