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* = Presenting author

P075 Innate immunity in inflammatory bowel disease and colon cancer

E. Lo Presti*1, R. Di Mitri2, F. Dieli1, F. Mocciaro2, G. Pecoraro2, G. Russo2, S. Meraviglia1

1University of Palermo, Central Laboratory of Advanced Diagnosis & Biomedical Research (CLADIBIOR), Department of Biopathology, Palermo, Italy, 2ARNAS Civico-Di Cristina-Benfratelli Hospital, Department of Gastroenterology and Endoscopy, Palermo, Italy


One of the most important consequences of chronically active inflammatory bowel disease (IBD) is the development of colorectal cancer (CRC) in a form called colitis-associated CRC (CAC) that significantly shows more aggressive features compared with sporadic CRC. It has been demonstrated that innate immune response plays a key role in inflammation-associated tumourigenesis, but little is known about the role of mucosal-associated invariant T (MAIT), innate lymphoid cells (ILC), and gamma-delta T-cells in sporadic and IBD-associated CRC. The aim of our study is to understand the contribution of several different components of innate immunity to inflammation-associated CRC.


We analysed 40 samples: IBD at onset (n = 10), IBD after therapy (n = 7), CRC (n = 16), CAC (n = 2), and healthy donors (n = 5). To identify specific lymphocyte subsets, immune cells were isolated from fresh intestinal biopsies, digested, and stained with fluorochrome conjugated monoclonal antibodies against intracellular and surface markers.


The frequency of type-1 innate lymphoid cells (ILC1) was higher in IBD (mean 20%), compared with CAC and sporadic CRC, and these infiltrating ILC1 produced high amounts of TNF-alpha but not IFN-gamma. IBD patients at onset also had higher frequencies of infiltrating Vdelta1 T-cells compared with CRC, whereas Vdelta 2 T-cells had an opposite pattern. Vdelta 1 T-cells produced IL-17 in sporadic CRC and IFN-gamma in IBD, whereas Vdelta 2 T-cells produced TNF-alpha and IFN-gamma in IBD and CRC, but IL-17 only in treated IBD patients. Interestingly, MAIT cells were present in CRC compared with IBD, whereas a very poor percentage was observed in healthy colon from the same patients.


Our results, albeit preliminary, suggest an appreciable and unexpected role for distinct subsets of innate lymphoid cells and MAIT cells in CAC, and provide a tool to evaluate the contribution of these subsets to the development of chronic inflammation-associated cancer.