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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 …
Contributors Study concept and design, JCH, AJC and FB. Acquisition of data, JCH, ML, WGH and BGD. Analysis and interpretation of data, JCH, AJC and NEN. Drafting of the manuscript, JCH, AJC, NEN and FB.
Funding This work was supported by the Gastroenterology Foundation of South Africa, the National Research Foundation (NRF, South Africa), the South African Research Chair Initiative. JCH is supported by CIDRI-Wellcome Trust (084323), Carnegie Corporation and an NRF Research Career Advancement fellowship.
Competing interests None declared.
Provenance and peer review Not commissioned; externally peer reviewed.