LAUSR

We read with great interest the review written by Fauny et al 1 which describes the relevance of interleukin-23/T-helper 17 (IL-23/Th17) pathway in inflammatory bowel disease (IBD). However, drugs targeting IL-17 have shown the opposite effect with worsening of the disease seen in patients with IBD leading to premature termination of various trials.2 3 Not only that, IL-17 inhibitors have also triggered new onset IBD in patients with spondyloarthritis. Consequently, the authors suggest a careful search for symptoms or family history of IBD as well as screening using faecal calprotectin levels in patients being planned for anti-IL-17 therapy. So far, the exact mechanism of this perplexing effect has not been elucidated and the authors have suggested that decreased intestinal barrier, predisposition to infection and subsequent inflammation may be responsible for worsening of IBD following anti-IL-17 therapy. We hereby describe other plausible pathways that can explain the same. Th17 cells were first described in 20054 by Langrish …