Effect of vanadium on human dendritic cells

Abstract

Vanadium is a heavy metal that has no known biological role in humans. However, increasing exposure through advances in medical applicationsorthodontic/orthopedic metal implants, vanadium-containing drugs and environmental exposure have raised questions on the influence of vanadium on the immune system. As initiators of the adaptive immune response, dendritic cells (DC) are responsible for the differentiation of effector T-lymphocytes and the resulting immune reactivity. This study assessed the differences in immune reactivity towards various vanadium compounds and investigated the influence of vanadium (III), (IV), and (V) ions on peripheral blood monocytes (PBMC) and DC. Exposure to vanadium (III) and (IV) concentrations above 125 mM reduced the proliferation of lymphocytes. Mitochondrial DC activity was reduced in the presence of low concentrations of vanadium. Flow cytometry analysis of cell surface molecules showed slight alterations of MHC class II (antigen presenting molecule) and reduction of CD54 (adhesion molecule) with increasing vanadium concentrations. Secreted cytokines and chemokines produced by DC were measured through a cytometric bead assay, which showed no significant difference after exposure to various vanadium ions. Finally, the ability of vanadium-treated DC to interact with lymphocytes was measured through proliferation of allogenic non-adherent PBMC and showed retention of proliferative capacity. These results indicate that vanadium exerts a weak influence on the maturation and function of DC, which suggests that alterations in immune reactivity by vanadium is mediated directly on effector lymphocytes.

CD11c decrease in mouse thymic dendritic cells after vanadium inhalation

“…The same outcomes were noted in our IHC analyses. Our results differ from those reported by Chan and Filgueira (2011) that found a discrete effect of V on DC maturation and function with any change in CD11c marker expression. We surmise that the differences compared to our results are because their work was done in vitro while ours was in vivo; specifically, Chan and Filgueira worked with human bone marrow cells (monocytes) that were induced to differentiate into DC before being cultivated with V, while we obtained our cells directly from the thymus of the V-exposed animals.…”

V4C3 MXene Immune Profiling and Modulation of T Cell‐Dendritic Cell Function and Interaction

“…In fact, the effect of other vanadium metallodrugs was limited to effector lymphocytes, without affecting the function of DCs. [ 56 ]…”

“…In fact, the effect of other vanadium metallodrugs was limited to effector lymphocytes, without affecting the function of DCs. [56] Subsequently, to evaluate also in murine immune cells whether the immunomodulation induced by the materials was independent from their cellular internalization, we performed TEM analysis upon MXene treatment in primary murine DCs and CD4 + T cells (Figure 4). For this purpose, DCs and CD4 + T cells, isolated from C57BL6 mouse spleens, were separately incubated with Ti 3 C 2 or V 4 C 3 (50 μg mL −1 ) for 24 h. Consistently with what observed for human PBMCs, V 4 C 3 was not taken up by either DCs or CD4 + T cells, while Ti 3 C 2 was clearly present in vacuolar structures inside DCs but not in CD4 + T cells (Figure 4).…”

“…[41,[51][52][53][54][55] Findings reveal that (III), (IV), and (V) vanadium ions influence the maturation and function of dendritic cells (DCs), thus affecting the immune response of effector lymphocytes. [56] Vanadium also modulates immune CD11c and MHC-II expression in thymic DCs by reducing CD11c surface marker expression. [57] This decrease may lead to T cell dysfunction, including possible negative selection.…”