A University of Tsukuba-based research team has shown that commensal bacteria in the gut can induce dendritic cells to release interferon-ß, which promotes Treg cell proliferation. However, apoptotic epithelial cells can inhibit this path through phosphatidylserine on their surfaces, which interacts with CD300a on dendritic cells and stops their production of interferon-ß. In this way, apoptotic epithelial cells can modulate the level of Treg cells.
This latest work builds on previous studies that have shown that beneficial bacteria, known as commensals, can modulate tissue status, including the effect they have on Treg cells. These cells are known to regulate immune activity, but details on this mechanism have never been clear. This issue is especially significant at barrier surfaces, such as in the gastrointestinal tract, where large numbers of epithelial cells detach and die via apoptosis. Prior to this study, it had also been unclear whether these dying cells had any particular effects.
Through a range of experiments, the research group showed that these dying, or apoptotic, cells in fact work to suppress proliferation of Treg cells. This is normally promoted by beneficial bacteria in the gut. The group also specifically identified the molecules involved—information that could be useful for treating diseases in which Treg cells are involved or are dysfunctional.
Dying Epithelial Cells Regulate the Immune System: Finding Could Aid Treatment of Inflammatory and Allergic Diseases