Dissecting the potential of resident CD11c-positive and CD11c-negative cells to support vitamin A-driven virus-specific immune responses in the upper respiratory tract (P6139)

Morbidity and mortality due to viral infections are major health concerns, particularly when individuals are vitamin A (VitA) deficient (VAD). Previous literature has suggested that CD11c+ dendritic cells in the gastrointestinal tract are largely responsible for VitA metabolism and the associated homing and function of gut lymphocytes. To determine if/how VitA impacts virus-specific immunity in the upper respiratory tract (RT), we administered virus intranasally (IN) to VAD mice. We found that virus-specific B- and T-cell responses were altered, with a significant down-regulation of IgA in the nasal wash of VAD mice compared to controls. We next asked if RT cells could autonomously support VitA-driven IgA production. We harvested CD11c+ and Cd11c- cells from diffuse nasal associated lymphoid tissues and found that both expressed RALDH mRNA, as required for VitA metabolism. Furthermore, preliminary data showed that both populations enhanced IgA in activated splenocyte cultures. To investigate which CD11c- cells were pertinent to function, we tested a RT epithelial cell line. These cells: (i) expressed RALDH mRNA and (ii) enhanced IgA in the presence of VitA A derivatives. In total, data highlighted the autonomous potential of RT cells to support a VitA-driven immune response. Results may ultimately instruct a clinical healthcare initiative to supplement VAD individuals with VitA by the oral or IN route, to enhance RT immunity toward viral infections and viral vaccines.