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The discovery of a new type of inflammatory cell1 would not feature in the wish list of a student of immunology grappling with the congested pathways of multiple cytokine molecules regulating a myriad of cell–cell interactions. However, the chest physician will be acutely aware that, with all our advanced knowledge of mechanisms underlying allergic asthma, there is clearly an unmet need for new therapy which will depend on further dissection of the cross-talk between immune and somatic cells in the lung. While the majority of patients with asthma respond to treatment with bronchodilator drugs and corticosteroids, others at the severe end of the spectrum are difficult to treat.2 These patients generate a substantial morbidity and socio-economic burden and asthma exacerbations carry a significant risk of fatal attacks.
The new cell type discovered by Petersen et al surfaced in the analysis of data from a model of chronic asthma in the mouse. Animal models, particularly in the mouse, have given us a working hypothesis that underpins the understanding of basic mechanisms of allergy. Data that build on, or deviate, from this provide new opportunities to develop novel therapy that may prove effective in difficult-to-treat asthma, where corticosteroid insensitivity is a particular problem. A major advance from studies of mouse models was the recognition of the polarisation of CD4 thymus-derived lymphocytes into T-helper (Th) 1 cells specialised to help defend against, …
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