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P095. Antibodies anti-interferon-inducible protein 16 (FI16) are elevated in inflammatory bowel diseases

L. Pastorelli1,2, V. Caneparo3, M. Bawadekar3, L.F. Pisani1, L. Spina2, G.E. Tontini2,4, M. Vecchi1,2, S. Landolfo5, M. Gariglio3, 1University of Milan, Department of Biomedical Sciences for Health, Milan, Italy, 2IRCCS Policlinico San Donato, Gastroenterology and Digestive Endoscopy Unit, San Donato Milanese, Italy, 3University of Piemonte Orientale, Department of Translational Medicine, Novara, Italy, 4University of Erlangen-Nuremberg, Medicine I, Erlangen, Germany, 5University of Turin, Department of Public Health and Microbiology, Turin, Italy

Background

The interferon-inducible protein 16 (IFI16) is a nuclear DNA sensor induced by several pro-inflammatory cytokines with various functions, including inflammation, innate immune response, and restriction of virus replication. It is a target for autoantibodies as specific antibodies have been demonstrated in the sera of patients with different inflammatory and autoimmune diseases. Aim of this study was to evaluate the prevalence of anti-IFI16 antibodies in inflammatory bowel disease (IBD) patients and their clinical significance.

Methods

Anti-IFI16 antibodies titers were measured in a cohort of 75 IBD patients' sera, including ulcerative colitis (UC, n = 27) and Crohn's disease (CD, n = 48), alongside with 182 healthy controls (HC), by means of an in house ELISA kit. Sera from those patients undergoing Infliximab (IFX) therapy were also collected before the first 5 drug infusions. Clinical data were collected and statistical analysis was performed using Student's t test or Fisher's exact test, as appropriate.

Results

Significantly higher levels of anti-IFI16 autoantibodies were observed in IBD patients compared to HC (mean levels ±SEM: 109.7±16.9 U/ml vs. 52.9±11.2 U/ml, p < 0.0001). Fifteen patients (20%) displayed anti-IFI16 and there was a trend towards a higher prevalence in UC vs. CD (25.9% vs. 16.6%). No correlation with biochemical or clinical disease activity was found. Anti-IFI16 levels were monitored for the first 5 drug infusions in a subgroup of 37 patients (12 UC and 25 CD) undergoing IFX therapy. The percentage of anti-IFI16 positive patients increased during IFX therapy from 18.9% to 70.2%. Interestingly, patients presenting anti-IFI16 antibodies at baseline or developing them during IFX therapy were more likely to be primary or secondary non-responder to IFX than those negative (34% vs. 0%, respectively; p = 0.03).

Table: Anti-IFI16 antibodies occurrences according with clinical response to IFX
Anti-IFI16 −Anti-IFI16 +
Responder to IFX1017
Primary/Secondary Non-responder to IFX9

Conclusion

Taken together, anti-IFI16 antibodies hold the potential to serve as a novel biomarker of disease and response to anti-TNF therapy in IBD.