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Cytokine networks in allergic lung inflammation: an opportunity for drug intervention.

Eosinophils and mast cells have long been considered as the major effector cells ultimately responsible for bronchial obstruction and airway hyper-responsiveness in asthmatics. However, there is now accumulating evidence that products of Th2 lymphocytes may orchestrate the generation, accumulation, and activation of these cells within the airway wall. Since the first report by Mosmannet al. in 1986 that murine helper T-cell clones could be divided into two subsets, Th1 and Th2, depending on their pattern of cytokine secretion, and observations that polarisation of Th1- or Th2-dependent cytokine production could be correlated with distinct autoimmune and allergic disorders, there has been an increasing interest in the possibility that pharmacological manipulation of the Th1/Th2 paradigm could provide novel treatments for human disease. This review summarises the evidence to date, attempts to explain some apparent discrepancies, and indicates opportunities for therapeutic intervention.