Emerging functional patterns of alpha-(2,6) sialylation in mucosal immunity

MOROSI, LUCIANO; MAHMOUD, YAMIL; MAY, MARÍA; MARIÑO, KARINA VALERIA; CUTINE, ANABELA; SASSO FERRER, MARIANELA; GATTO, SABRINA; TOSCANO, MARTA A; MARTINEZ ALLO, VERONICA; MORALES, ROSA; RABINOVICH, GABRIEL A.

Los Cocos, Córdoba, Argentina

Simposio; Advanced Course on Mucosal Immunology (ACMI 2018), Society of Mucosal Immunology; 2018

Society of Mucosal Immunology

Inflammatory bowel diseases (IBD), such as ulcerative colitis and Crohn´s disease, are characterized by chronic inflammation of all or part of the digestive tract. The etiology of IBD probably involves a combination of genetic predisposition and environmental factors that may be channeled through an abnormality in gut-barrier function, with the loss of immune tolerance. One of the early features of IBD is basal plasmacytosis, there is an elevated number of plasma cells (PCs) infiltrating gut lamina propria. Gut PCs physiologically produce high amounts of the heavily glycosylated dimeric IgA that is translocated to the gut lumen through the epithelium, during this process the secretory component is covalently attached to the IgA dimer. Secretory IgA (sIgA) exerts a diversity of functions, these include neutralizing toxins and viruses, blocking excessive live bacterial adherence or translocation and directed sampling of luminal antigen. PCs have recently regained attention in IBD due to the interplay between secretory IgA (sIgA) and dysbiosis in IBD patients, however, their role in these pathologies is still far from clear. Evidence shows that mucosal glycosylation is altered during IBD both in cell surface (e.g. T-cells, epithelial cells) and secreted glycoconjugates (e.g. mucins), influencing glycan-associated programs that modulate immune responses and microbiota composition. Conversely, there is still a lack of information regarding PCs and sIgA glycosylation in IBD and the potential impact on their functionality. Thus, the aim of this work is to study the glycome of lamina propria PCs in physiologic and inflammatory conditions, and the potential impact of these alterations in experimental models of colitis.