Viral-induced T helper type 1 response enhance allergic disease by effects on lung dendritic cells

Nat. Immunol. 5, 337-343(2004)

Speaker: 蔡明怡

Commentator: 余俊強 老師

Time: 13:00-14:00 April 14, 2004

Place: Room 601

Abstract:

    Asthma is a chronic disease of the lung characterized by reversible airway obstruction and hyper-responsiveness and is associated with pulmonary inflammation. Classically, asthma is thought to arise from an imbalance in T_H1-T_H2 immune regulation, resulting in increased T_H2 cytokines, IL-4, IL-5and IL-13, as well as augmented immunoglobulin E production and pulmonary eosinophilia.  It is widely accepted that T_H1 cytokines such as IFN-γ antagonize allergic disease mediated by T_H2 cytokines.  The ‘hygiene hypothesis’ proposes that the T_H2 cytokines increase reflect a reduction in the exposure of children to bacterial and viral pathogens that are believed to be protective against asthma (1).  Some experiments in mice supported the idea that T_H1 immune response may inhibit T_H2-mediated disease in a non-antigen-specific way (2).  However, the long-term effects of T_H1 responses induce as part of natural infections on allergic disease remain unclear.  Here, the Author showed that influenza A infection incites a robust IFN-γ response in the lung, promoting the development of durable, T_H1-polarizing dendritic cells (DCs).  These DCs bolstered subsequent immunity in T_H2-dependent mouse model of allergen-induced lung inflammation, enhancing both T_H1 and T_H2 immune cytokines and immunoglobulin production.  Contrary to the hygiene hypothesis, this study demonstrated that respiratory infection with influenza A virus is not protective but rather enhances the development of allergic disease.  This effect is mediated at least in part by IFN-dependent alterations on lung DCs.

Reference:

1.      Wills-Karp, M., Santeliz, J. & Karp, C.L. The germless theory of allergic disease:revisiting the hygiene hypothesis. Nat. Rev. Immunol. 1, 69–75 (2001).

2.      Lewis, D.B. Allergy immunotherapy and inhibition of Th2 immune responses: a sufficient strategy? Curr. Opin. Immunol. 14, 644–651 (2002).