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Chronic inflammatory disease is generally thought to be the result of an altered adaptive immune response. This paper describes a novel innate immune pathway driven by persistent viral infection.
A mouse model of chronic inflammatory lung disease was generated by a viral infection which produced mucous cell metaplasia and airway hyper-responsiveness. Maximal airway disease activity coincided with a peak of CD1d-dependent T cell receptor-invariant natural killer T (NKT) cell recruitment of macrophages as well as peak interleukin (IL)13 levels in the lungs. This cellular interaction was independent of CD4+ T cells which were previously thought to be the focus of a response to allergens in the lungs.
It has long been suggested that common respiratory viruses are central to the development of chronic airway inflammation in asthma, particularly in children. However, it is not clear how this could occur many years after the apparent clearance of the infection. Interestingly, this report shows that the virus initiating the airway damage remains detectable in the lung in trace amounts, and further studies will be needed to establish the relevance of persistent infection in those with chronic obstructive pulmonary disease.
The discovery of this new immune axis suggests that the recruitment and persistent activation of IL13 producing macrophages by NKT cells in human lung tissue may be involved in the development of chronic lung disease.
▸ Kim EY, Battaile JT, Patel AC, et al. Persistent activation of an innate immune response translates respiratory viral infection into chronic lung disease. Nat Med 2008;14:633–9
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