Anti-tumor necrosis factor-α therapy and paradoxical autoimmunity in inflammatory bowel disease: a need for risk-aware monitoring

than simply accumulating as a late complication of prolonged therapy.These findings are consistent with previous evidence that TNF inhibitors may be associated with immune-mediated inflammatory diseases in patients with IBD. 5 Among these events, psoriasis is the most consistently recognized paradoxical manifestation, with systematic review data showing a meaningful incidence of psoriasis or psoriasiform lesions among IBD patients receiving anti-TNF therapy. 6A Korean nationwide cohort study also demonstrated an increased risk of psoriasiform disease after TNF antagonist exposure, supporting the relevance of this signal in Korean patients with IBD. 7 Mechanistically, anti-TNF-induced psoriasiform lesions in IBD have been linked to Th1 and Th17 inflammatory pathways, supporting the concept that TNF blockade may redirect rather than simply suppress immune activity. 8,9The ILD signal reported by Oh et al. 4 is also clinically important, although it should be interpreted cautiously.TNF-targeted therapies have previously been reported to induce or exacerbate ILD, but establishing causality is difficult because infection, underlying immune-mediated disease, and pre-existing lung involvement may confound clinical interpretation. 10Nevertheless, new respiratory symptoms during anti-TNF-α therapy should prompt careful evaluation rather than being attributed automatically to infection or nonspecific pulmonary complaints.