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Interleukin 13-mediated colitis in the absence of IL-4Rα signalling
  1. Jennifer C Hoving1,2,
  2. Antony J Cutler1,2,3,
  3. Mosiuoa Leeto1,2,
  4. William G C Horsnell1,2,
  5. Benjamin G Dewals1,2,4,
  6. Natalie E Nieuwenhuizen1,2,5,
  7. Frank Brombacher1,2
  1. 1International Centre for Genetic Engineering and Biotechnology (ICGEB), Cape Town Component, Cape Town, South Africa
  2. 2Division of Immunology, Institute of Infectious Diseases and Molecular Medicine (IDM), Faculty of Health Sciences, University of Cape Town and South African Medical Research Council (SAMRC), Cape Town, South Africa
  3. 3JDRF/Wellcome Trust Diabetes and Inflammation Laboratory, Wellcome Trust Centre for Human Genetics, Nuffield Department of Medicine, University of Oxford, UK
  4. 4Fundamental and Applied Research in Animals and Health, Faculty of Veterinary Medicine, University of Liege, Belgium
  5. 5Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany
  1. Correspondence to Professor Frank Brombacher or Jennifer C Hoving, International Centre for Genetic Engineering and Biotechnology (ICGEB) University Campus, Room S1.27/S1.21, Werner Beit South Wing, Observatory 7925, Cape Town 7925, South Africa; brombacherfrank{at}gmail.com, jennifer.hoving{at}uct.ac.za

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Sufficient evidence points to interleukin 13 (IL-13) as an important pathological factor in UC and raises hopes to a promising new treatment strategy.1–3 However, the outcomes of two recent clinical trials, both published in Gut 2015, suggest otherwise.4 ,5 A commentary published in the same issue described these results as crushing the enthusiasm for anti-IL-13 treatment in UC.6 In this letter, we show evidence that the disease outcome is determined by the type of signalling pathway used by IL-13 in mice. Therefore, we suggest that directly blocking IL-13 remains a potential treatment strategy for a subset of patients with UC that have elevated tissue IL-13 production.

In the first clinical study using anrukinzumab treatment, which targets the IL-4 receptor-alpha (IL-4Rα) and not IL-13 directly, had no effect on improving the clinical response or remission rates of patients with UC.4 In contrast, although patients treated with tralokinumab, which blocks IL-13 directly, showed no improved clinical response rate, there was …

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