TY - JOUR T1 - Mucosa-associated microbiota drives pathogenic functions in IBD-derived intestinal iNKT cells JF - Life Science Alliance JO - Life Sci. Alliance DO - 10.26508/lsa.201800229 VL - 2 IS - 1 SP - e201800229 AU - Claudia Burrello AU - Gabriella Pellegrino AU - Maria Rita Giuffrè AU - Giulia Lovati AU - Ilaria Magagna AU - Alice Bertocchi AU - Fulvia Milena Cribiù AU - Francesca Boggio AU - Fiorenzo Botti AU - Elena Trombetta AU - Laura Porretti AU - Antonio Di Sabatino AU - Maurizio Vecchi AU - Maria Rescigno AU - Flavio Caprioli AU - Federica Facciotti Y1 - 2019/02/01 UR - https://www.life-science-alliance.org/content/2/1/e201800229.abstract N2 - Inflammatory bowel disease (IBD) pathogenesis has been linked to the aberrant activation of the Gut-associated lymphoid tissues against components of the intestinal microbiota. Although the contribution of CD4+ T helper cells to inflammatory processes is being increasingly acknowledged, the functional engagement of human invariant natural killer T (iNKT) cells is still poorly defined. Here, we evaluated the functional characteristics of intestinal iNKT cells during IBD pathogenesis and to exploit the role of mucosa-associated microbiota recognition in triggering iNKT cells’ pro-inflammatory responses in vivo. Lamina propria iNKT cells, isolated from surgical specimens of active ulcerative colitis and Crohn’s disease patients and non-IBD donors, were phenotypically and functionally analyzed ex vivo, and stable cell lines and clones were generated for in vitro functional assays. iNKT cells expressing a pro-inflammatory cytokine profile were enriched in the lamina propria of IBD patients, and their exposure to the mucosa-associated microbiota drives pro-inflammatory activation, inducing direct pathogenic activities against the epithelial barrier integrity. These observations suggest that iNKT cell pro-inflammatory functions may contribute to the fuelling of intestinal inflammation in IBD patients. ER -