The University of Virginia researchers used healthy mice and mice genetically engineered to lack aryl hydrocarbon receptor (AHR) in CD4-positive T-cells, an immune cell type implicated in MS, in the first set of experiments. These animals were subjected to the standard protocol for inducing an MS-like disease called experimental autoimmune encephalomyelitis (EAE). The results showed that mice lacking AHR had the same time to disease onset and peak clinical severity as healthy mice, but recovered faster in the chronic phase. The difference in recovery was only observed when the mutant mice were housed separately from their healthy counterparts, according to the researchers. The team hypothesized that this was due to microbiome differences that were only apparent when the mice lived separately and did not influence each other’s microbiomes.