Despite the advancements in vaccination research and practices, influenza viruses remain a global health concern. Inducing a robust immune response by vaccination is especially challenging in the elderly, the immunocompromised, and persons with chronic illnesses. Polysaccharides derived from food may act as a safe and readily accessible means to boost the immune system during vaccination. In this study, we investigated whether crude polysaccharides derived from carrot pomace (CPP) could stimulate innate immune cell function and promote influenza vaccine immunogenicity. In bone marrow-derived dendritic cells (BMDCs), CPP increased the fraction of CD11c+MHCII+ cells and the expression of co-stimulatory molecules CD40 and CD80, indicative of enhanced maturation and activation. Functionally, CPP-treated BMDCs promoted inflammatory cytokine production in splenic lymphocytes. In a mouse model of immunosuppression induced by cyclophosphamide, animals given CPP before and after an influenza vaccine challenge showed increased frequencies of dendritic cells and natural killer cells in the spleen, in addition to the recovery of vaccine-specific antibody titers. Moreover, innate myeloid cells in CPP-fed mice showed evidence of phenotypic modification via markedly enhanced interleukin(IL)-12 and interferon(IFN)-γ production in response to lipopolysaccharide(LPS) stimulation ex vivo. Our findings suggest that the administration of carrot pomace polysaccharides can significantly enhance the efficacy of influenza vaccination.

Rheumatoid arthritis (RA) is a common autoimmune disease characterized by immune cell infiltration of the synovium, leading to the loss of cartilage, bone, and joint function. Although regulatory T (T_reg) cells are thought to modulate the initiation and progression of RA, a consensus has yet to be reached regarding the function and composition of T_reg cells in RA patients. To address these discrepancies, we analyzed not only the total T_reg frequency but also that of T_reg subpopulations in the peripheral blood of RA patients and healthy controls by flow cytometry. We found that the total T_reg population was not significantly different between RA and control subjects. However, the effector T_reg cell subgroup, defined as CD45RA⁻CD25^hi, showed markedly decreased frequency in RA patients. In addition, the total T_reg population from RA patients showed a significant decline in the expression of CD25. Both the naïve and effector T_reg subgroups also showed marked reduction of CD25 expression in RA patients compared to controls. These data suggest that the decreased frequency of effector T_reg cells and overall reduction of CD25 expression in T_reg cells in the peripheral blood may be evidence of altered T_reg homeostasis associated with RA pathogenesis.