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Recent data strongly support the view that coeliac disease is a Th1 mediated inflammatory disease as both interferon γ production and T-bet levels in gut infiltrating cells are upregulated
The puzzling observation on high interferon γ (IFN-γ) but low interleukin (IL)-12 levels in coeliac disease (CD) has resulted in questions about the underlying principles of T helper cell polarisation. In this issue of Gut,1 the molecular basis of T helper cell polarisation in CD has been illuminated by the finding that T-bet, the master transcription factor of T helper cell type 1 (Th1) cells, is upregulated in this disease [see page 1090].
The past decade has witnessed a dramatic improvement in our pathophysiological understanding of inflammatory disorders of the intestinum due to extensive research efforts focusing on regulatory mechanisms of the immune system. This has been greatly facilitated by the advent of molecular biological techniques which have allowed for the identification and characterisation of distinct factors in the complex regulatory network of the immune system. General themes have thus been recognised and an attempt is being made to classify diseases according to common immunological features.
One crucial emerging theme is the Th1/Th2 polarisation of T helper cells.2,3 On activation with distinct immunological stimuli, naive CD4+ precursor T helper cells differentiate into mature T cells which either produce a so called Th1 cytokine profile characterised by tumour necrosis factor α (TNF-α) and IFN-γ, or a T helper cell type 2 (Th2) cytokine profile including IL-4, IL-5, IL-9, and IL-13. While these T cell subsets produce proinflammatory cytokines that can cause substantial tissue injury in vivo, more recent data suggest that additional subsets of CD4+ T helper cells exist with anti-inflammatory functions. These subsets include T helper 3 (Th3) cells producing transforming growth …
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