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inflammatory bowel disease (IBD)



  • mechanisms are not well understood as yet
  • Hepworth et al 1) propose the following mechanism:
    • a subset of innate lymphoid cells called ILC3 cells which normally reside in the lamina propria of the bowel and in mesenteric lymph nodes, selectively kill CD4 T cell lymphocytes that are capable of responding to bacterial antigen originating from the gut.
    • normally these ILC3 cells prevent the immune system from mounting an inflammatory response to these non-pathogenic bacteria gut flora in a similar way as thymic medullary epithelial cells or dendritic cells of the thymus kill off specific CD4 T cells to reduce the risk of auto-immune diseases
    • biopsies of children with Crohn's disease reveal a deficiency in the expression of ILC3-instrinsic MHC class II suggesting this could be a key component of the pathogenesis

pharmacologic Rx options

  • sulphasalazine (salazopyrine)
  • TNF antagonists
  • monoclonal antibodies to integrin:
    • iv vedolizumab every 8wks (introduced in Australia in 2015)
NEJM 373;24 Dec 10 2015 and Science 2015; 348:1031-5;
ibd.txt · Last modified: 2016/01/11 08:49 by

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