An active form of vitamin D can modulate the activity of immune cells and prevent autoimmune reactions known to be involved in several human diseases such as multiple sclerosis (MS).
A study with that finding, led by researchers from The University of Edinburgh in Scotland, reveals a new layer of knowledge that may help better understand the role of vitamin D in human health and disease.
The study “1,25-Dihydroxyvitamin D3 Restrains CD4+ T Cell Priming Ability of CD11c+ Dendritic Cells by Upregulating Expression of CD31,” was published in the journal Frontiers in Immunology.
“Low vitamin D status has long being implicated as a significant risk factor for the development of several autoimmune diseases,” Richard Mellanby, PhD, said in a press release. Mellanby is principal investigator at the Centre for Inflammation Research from the University of Edinburgh, and senior author of the study, “Our study reveals one way in which vitamin D metabolites can dramatically influence the immune system,” Mellanby said.
The human immune system relies on complex interactions between several groups of cells, in order to achieve the best protective shield against threats, while preserving the body’s healthy cells and tissues.
An important step of this process is the maturation of immune T-cells, which are the main active immune cells responsible for detecting and destroying whatever may put the body in danger.
T-cells need to learn what may represent a threat and what belongs to the body, and for this they rely on another group of “teaching” cells called dendritic cells. When this process is altered, T-cells may start to target their surroundings indiscriminately, promoting damage to the body’s own cells, and leading to the development of autoimmune diseases.
Researchers found that an active form of vitamin D, called 1,25-dihydroxyvitamin D3, also may contribute for this teaching process of T-cells. This vitamin D metabolite can reshape the genetic profile of dendritic cells, promoting the presence of the surface receptor CD31.
When the levels of CD31 were increased, dendritic cells were unable to support the activation of T-cells. In contrast, when researchers genetically manipulated dendritic cells to lack CD31, these cells had an increased potential to activate T-cells.
The team also found that CD31 had this inhibitory effect by preventing prolonged contact between dendritic cells and T-cells, in both human and mouse-derived cells.
“Exposure of bone marrow dendritic cells (BMDC) during development to 1,25-dihydroxyvitamin D3 is critical in the upregulation of inhibitory pathways which further restrain the ability of BMDC to prime [activate] T-cells,” researchers wrote.
Overall, the findings suggest that in the presence of this active vitamin D metabolite, dendritic cells may retain a more tolerant status, and subsequently suppress T-cell mediated autoimmune reactions.
Additional studies are warranted to further explore ways to use CD31 in dendritic cells as a strategy to lessen the activation of T-cells.