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Gene expression of IL17 and IL23 in the lungs of patients with active tuberculosis
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  1. K Dheda1,2,
  2. J-S Chang1,
  3. S Lala3,
  4. J F Huggett1,
  5. A Zumla1,
  6. G A W Rook1
  1. 1Lung Infection and Immunity Unit, CTBRI, Division of Pulmonology, Department of Medicine, University of Cape Town and Groote Schuur Hospital, Observatory Cape Town, South Africa
  2. 2Centre for Infectious Diseases and International Health, Division of Infection and Immunity, Royal Free and University College Medical School, University College London, London, UK
  3. 3Centre for Gastroenterology, Royal Free and University College Medical School and Royal Free Hospital NHS Trust, London, UK
  1. Dr K Dheda, Centre for Infectious Diseases and International Health, Division of Infection and Immunity, Royal Free and University College Medical School, University College London, 43 Cleveland Street, London, W1T 4JF, UK; keertandheda{at}yahoo.co.uk

https://doi.org/10.1136/thx.2007.092205

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    Immunity to tuberculosis is dependent on type 1 responses (interferon (IFN)γ, interleukin (IL)12, tumour necrosis factor (TNF)α) but these do not provide a complete explanation for the regulation of the immune response seen. Additional effector or regulatory mechanisms need to be sought.1 Recently, a new T cell subset, IL-17 producing CD4+ Th cells (Th17), has been described.2 In the mouse at least, IL-17 secreting cells may be distinct from conventional Th1, Th2 and regulatory T cells.2 These IL-17-secreting T cells drive secretion of TNFα, IL1β and IL6, as well as chemokines CXCL1, 2 and 8, and enhance inflammation and influx of neutrophils.2 IL17 has tentatively been implicated in mouse models of immunity to mycobacteria.3 ,4 However, there are no data from the human lung or from patients with tuberculosis (TB). …

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