DIFFERENTIAL GLYCOPPATERNS OF GUT-ASSOCIATED B CELLS IN PHYSIOLOGICAL AND INFLAMMATORY CONDITIONS.

ANABELA M. CUTINE,; LUCIANO G. MOROSI; VERÓNICA C. MARTINEZ ALLO; ROSA MORALES; GABRIEL A. RABINOVICH,; MARTA A. TOSCANO ; KARINA V. MARIÑO

Buenos Aires

Congreso; Primer Congreso Internacional conjunto LASID-SAI-FAIC.; 2015

LASID-SAI-FAIC.

Background.Crohn´s disease and ulcerative colitis are chronic inflammatory intestinal diseases, often collectively referred as inflammatory bowel diseases (IBD); in spite of their high incidence, characterization of the molecular pathways involved in their onset and development is far from complete. With an interdisciplinary approach to IBD, we are investigating how specific glycans (generated and/or modified during the transition from healthy to inflamed mucosa) can mediate cellular processes relevant to immune tolerance and inflammation. In this study we focus on characterizing theglycophenotype of B cells isolated from the gut and its response to local inflammation in experimental models of colitis.Methods.We purified lymphocytes from different gut associated lymphoid tissues inC57BL6/J mice. To study the potential glycome modulation byinflammatory conditions, we used the 2,4,6-Trinitrobenzenesulfonic acid (TNBS)-induced colitis model. B cellglycophenotypewas characterized using biotinylatedlectinsand flow cytometry.Results.B cells from the lamina propria show a glycophenotype rich in complex N-glycans and α2,6sialic acid, in opposition toB cells isolated from theappendix and Peyer Patches. Under inflammatory conditions, there is a differential modification in the level ofcomplexN-glycansin B cells from lamina propria, and in α2,6sialylation in B cells from mesenteric lymph nodes.Conclusions. B cells from gut associated lymphoid tissues exhibit a modulation of their surface glycophenotype depending on location and inflammatory status. These differences could be relevant to the physiological function of B cells in different compartments, but they could also play a part in the pathogenesis of IBD.