To respond or not to respond: T cells in allergic asthma

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Abstract
There has been an epidemic rise in the incidence of atopic disease, including allergic asthma, over the past few decades. CD4+ T helper 2 (TH2) cells are the prime mediators of allergic airway inflammation, including eosinophilia and mucus hypersecretion. TH2-cell driven allergic inflammatory responses in the lung require innate immune signals — for example through the Toll-like receptors (TLRs). The dose of pathogen-associated molecular pattern (PAMP) exposure regulates the induction of TH2- versus TH1-type inflammation. TH1 effector T cells do not prevent and might exacerbate lung inflammatory responses. Various types of CD4+ regulatory T cells have been identified that can limit unwanted adaptive immune responses. The link between decreased exposure to infectious agents in early life and the increased incidence of atopic disease (hygiene hypothesis) may be explained by a failure to generate regulatory T-cell populations. Regulatory T cells have been implicated in suppression of airway inflammation. Innate immune system signals, such as those delivered through TLRs, have an important role both in the generation of adaptive immune responses and regulatory T cells.