Neurogenic niches are important spots into the brain in which neural stem cells and other homeostatic populations harbour, and in which neurogenesis takes place. One of their well-renown limits is represented by the fact that, as years pass by, niches become less-functional, and neural regeneration becomes less efficient. RNA sequencing-based single-cell analysis, performed by Dulken and collaborators, individuated, for the first time, a clonally-expanded population of CD8+ T cells in older mice that might be responsible of loss of efficiency of the neural progenitors in the niches. These lymphocytes display a different transcriptomic fingerprint from those found in the periphery, they are almost absent in younger animals and express gamma-interferon (IFNg), by means of which they seem to be able to suppress proliferation in the interferon-responding neurons of the neurogenic niches.
The authors used BTS2, the mouse orthologous gene of human tetherin, as a surface marker to individuate interferon response signature in niche-resident activated neural stem cells (aNSCs) and neural progenitor cells (NPCs). BTS2-expressing aNSCs/NPCs from old mice displayed significant depletion of cell cycle-related mRNAs, indicating that they were less prone to replicate and initiate neurogenesis in presence of IFNg-producing cells. This was further corroborated by the fact that higher amounts of BTS2-expressing cells in neurogenic niches correlated with the amount of T cells, while experimentally-induced entry of CD8+ T cells in the brain enhanced the amounts of BTS2-positive neuron progenitors, as well as reducing their proliferative capacity.