P054 Innate lymphoid cells in paediatric inflammatory bowel disease

• Published in: Journal of Crohn's and colitis 2018-01, Vol.12 (supplement_1), p.S119-S120
• Main Authors: Van Acker, A, Kvedaraite, E, Lourda, M, Ideström, M, Henter, J -I, Svensson, M, Mjösberg, J
• Format: Article
• Language: English
• ISSN: 1873-9946; 1876-4479
• DOI: 10.1093/ecco-jcc/jjx180.181

Abstract Background The incidence of paediatric IBD (PIBD) is on the rise. However, the underlying aetiology of PIBD remains largely unknown, indicating the dire need for more knowledge on the mechanisms driving this disease. Innate lymphoid cells (ILCs) constitute an important component of the mucosal immune system. Recent years have seen an increase in ILC knowledge, with numerous publications highlighting the importance of ILCs in murine and adult IBD development and progression. In this project, we aim to elucidate ILC heterogeneity and function specifically in PIBD. Methods Peripheral blood mononuclear cells (PBMCs) and single-cell suspensions were isolated from blood and colon biopsies, respectively, of 17 PIBD and 4 non-PIBD patients admitted to the Paediatric Gastroenterology, Hepatology and Nutrition Unit at Karolinska University Hospital, Stockholm, Sweden. ILC population frequency and phenotype was examined by 18-colour flow cytometry and correlated to children’s IBD physician global assessment (PGA) scores. Results Our results show a statistically significant decrease in the frequency of ILC3 cells (p < 0.05) and a statistical tendency towards an increase in the frequency of ILC1 (p = 0.06) in the gut of PIBD as compared with non-PIBD control patients. In PBMC, we detected a slight decrease in the frequency of ILC1 (p = 0.06). Conclusions Our data suggest a skewing of the ILC balance in the intestinal mucosa of PIBD patients, with an increase of IFNγ producing ILC1, and a decrease of IL-22 producing ILC3. These data mirror those from adult IBD, where ILC1 accumulate in the intestine of both CD and UC patients. However, our results are based on a small patient cohort and as yet lack sufficient power for our intended statistical analysis. Extensive further research will now be conducted to continue this analysis as well as examine additional phenotypical and functional differences in ILCs from PIBD patients and non-PIBD controls as this might generate novel insights into disease mechanisms and future treatment targets.