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Th2 cytokines and asthma: an introduction

Peter J Barnes

National Heart & Lung Institute, Imperial College, Dovehouse Street, London SW3 6LY, UK

corresponding author email

Respiratory Research 2001, 2:64-65doi:10.1186/rr39

Published: 8 March 2001

First paragraph (this article has no abstract)

Asthma is a highly complex disease that is still poorly understood and whose cause remains unknown. One of the striking advances in the last decade has been the recognition that cytokines play a critical role in orchestrating, perpetuating and amplifying the inflammatory response in asthma. Indeed the increased and abnormal expression of cytokines in airway cells is one of the major targets of corticosteroid therapy, by far the most effective controller treatment for asthma currently available. Many cytokines and chemokines are involved in the pathophysiology of asthma [1,2]. While some of these cytokines, such as interleukin (IL)-1, tumour necrosis factor-α and IL-6, are involved in many inflammatory diseases, including chronic obstructive pulmonary disease, rheumatoid arthritis and inflammatory bowel disease, others are more specific to allergic inflammation. These cytokines, IL-4, IL-5, IL-9 and IL-13, are derived from T helper type 2 (Th2) cells, although they may also derive from other cell types. Th2 cells are recognised by their secretion of IL-4, IL-5, IL-9 and IL-13, as opposed to Th1 cells, which secrete IL-2 and interferon-γ, although the clear distinction between Th1 and Th2 cells is not as distinct in humans as in mice. Th2 cytokines may play an important role in the pathophysiology of allergic diseases, including asthma. They may be useful therapeutic targets in the future management of allergic diseases, and several approaches to inhibiting these cytokines are now being tested in clinical trials or are in active development [3].


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