The complex etiology of IBD results from inherent genetic disposition and from the multifactorial crosstalk between the inﬁltrating immune cells and the inﬂamed epithelium. As such, standard treatment for moderate to severe IBD patients relies on timely and eﬀective intervention with the immune cell-driven inﬂammation. Patients that become refractory to steroids and immunosuppressants (5-ASA, mesalamine, and azathioprine) are subsequently treated with biologics such as tumor necrosis factor alpha (TNFα) blockers, including inﬂiximab, adalimumab, etanercept, and certolizumab pegol . Although TNFα inhibition is one of the most common therapies for refractory IBD patents, up to 40% of patients treated in such way manifest primary unresponsiveness (UR) shortly after the initial dose, whereas 23-46% patients experience gradual loss-of-response (LOR) within 6-12 months of treatment . The relatively high incident of treatment failure and the lack of durable clinical response to TNFα therapy emphasizes the need to better dissect causalities of TNF refractoriness in IBD.
|Effective start/end date||6/1/22 → 5/31/23|
- Kenneth Rainin Foundation (20220023)
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