1. ¹Centre for Functional Genomics and Human Disease, Monash Institute of Medical Research, Monash University, Parkville, Victoria, Australia
2. ²Cooperative Research Centre for Chronic Inflammatory Disease, Parkville, Victoria, Australia
3. ³School of Applied Sciences and Engineering, Monash University, Churchill, Victoria, Australia
4. ⁴Division of Infectious Diseases and Immunology, University of Massachusetts Medical School, Worcester, MA, USA

Correspondence: Professor PJ Hertzog, Centre for Functional Genomics and Human Disease, Monash Institute of Medical Research, 27-31 Wright Street, Clayton, Victoria 3168, Australia. E-mail: Paul.Hertzog@med.monash.edu.au

Received 13 June 2007; Accepted 14 June 2007; Published online 31 July 2007.

Abstract

Recent advances in unravelling the complexities of the signalling pathways that constitute innate immunity have highlighted type I interferon as a key component in the response to infection. Here we focus on the emerging field of pattern-recognition receptor signalling, specifically Toll-like receptors and retinoic acid inducible gene-like helicases, from the perspective of this 50-year-old cytokine. The type I interferon gene family encompasses more than 20 subtypes, whose nature and properties have been extensively studied during its relatively long history. In this review we update and integrate available data on the mechanics of activation of the interferon genes and the role of this cytokine family in the innate immune response.