This was not observed in KO mice. LF persistence within the gut was improved in KO mice,leading to aggravated intestinal inflammation,compared to that in WT mice. Depletion of GCN didn’t have an effect on susceptibility of mice to DSSinduced colitis,indicating that the effects obtained were not a consequence of inflammation and have been precise for AIEC infection. Conclusion: The GCNeIFATF pathway is activated in host cells through AIEC infection,which can be served as a defense mechanism to induce a functional autophagy to manage AIEC intracellular replication. Disclosure of Interest: None declaredUnited European Gastroenterology Journal (S) significance of this cell population. Due to the fact Vitamin D has an immunosuppressive impact on immune cells,we wanted to establish the role of vitamin D in antiTNF induced macrophages. The aim of this study was to figure out if the Vitamin D receptor pathway was activated in antiTNF induced macrophages and if Vitamin D can potentiate immunosuppressive impact of these macrophages. Aims Methods: Peripheral blood mononuclear cells (PBMC) had been isolated from peripheral blood of healthful donors. MLR had been established by coculturing PBMC of two wholesome donors within a : ratio. Cultures were treated with antiTNF to induce antiTNF induced macrophages. IFNinduced macrophages were generated by culturing monocytes inside the presence of IFN. Gene expression of antiTNF in comparison to IFNinduced macrophages was determined by microarray or by realtime PCR. Protein expression in the Vitamin D receptor (VDR) was determined by western blot. To identify the effect of Vitamin D on IFNand antiTNF induced macrophages cell culture experiments had been performed inside the presence or absence of .dihydroxyvitamin PubMed ID: D. AntiTNF induced macrophages have been isolated with CD microbeads and cocultured with activated Tcells from a third donor. Subsequently Tcell proliferation was measured by H thymidine incorporation. Outcomes: AntiTNF induced macrophages displayed improved expression of a number of components on the vitamin D receptor pathway like the transcripts for VDR,Osteopontin and the Retenoid X receptor. In line with this,antiTNF induced macrophages showed improved VDR protein expression when compared with IFNinduced macrophages,confirming the outcomes of the micro array. Moreover antiTNF induced macrophages showed enhanced expression in the VDR response gene cathelicidin antimicrobial peptide soon after therapy with .dihydroxyvitamin D. Indicating enhanced capacity to respond to Vitamin D. As a way to identify if Vitamin D could improve the immunosuppressive impact of antiTNF induced macrophages,macrophages have been generated inside the presence of the Salvianolic acid B active metabolite of vitamin D. Addition of active vitamin D did not alter the amount of regulatory macrophages. Having said that antiTNF induced macrophages generated inside the presence of .dihydroxyvitamin D did show an increased capacity to inhibit of Tcell proliferation. Conclusion: AntiTNF induced macrophages show an improved activation in the vitamin D receptor pathway. The immunosuppressive properties of antiTNF induced macrophages is usually potentiated by .dihydroxyvitamin D. Disclosure of Interest: A. Levin: None declared,M. Wildenberg: None declared,P. Koelink: None declared,F. Bloemendaal: None declared,G. D’Haens Conflict with: has served as speaker,consultant,and principal investigator for AbbottAbbVie,AM Pharma,CentocorJanssen Biologics,Engene,Photopill,Setpoint,Novo Nordisk,MSD,UCB,Takeda,TEVA,Millenium,Boehringer Ingelheim,El.