6 research outputs found
Heavy-tailed kernels reveal a finer cluster structure in t-SNE visualisations
T-distributed stochastic neighbour embedding (t-SNE) is a widely used data
visualisation technique. It differs from its predecessor SNE by the
low-dimensional similarity kernel: the Gaussian kernel was replaced by the
heavy-tailed Cauchy kernel, solving the "crowding problem" of SNE. Here, we
develop an efficient implementation of t-SNE for a -distribution kernel with
an arbitrary degree of freedom , with corresponding to SNE
and corresponding to the standard t-SNE. Using theoretical analysis and
toy examples, we show that can further reduce the crowding problem and
reveal finer cluster structure that is invisible in standard t-SNE. We further
demonstrate the striking effect of heavier-tailed kernels on large real-life
data sets such as MNIST, single-cell RNA-sequencing data, and the HathiTrust
library. We use domain knowledge to confirm that the revealed clusters are
meaningful. Overall, we argue that modifying the tail heaviness of the t-SNE
kernel can yield additional insight into the cluster structure of the data
Human retinoic acid-regulated CD161+ regulatory T cells support wound repair in intestinal mucosa.
Repair of tissue damaged during inflammatory processes is key to the return of local homeostasis and restoration of epithelial integrity. Here we describe CD161+ regulatory T (Treg) cells as a distinct, highly suppressive population of Treg cells that mediate wound healing. These Treg cells were enriched in intestinal lamina propria, particularly in Crohn's disease. CD161+ Treg cells had an all-trans retinoic acid (ATRA)-regulated gene signature, and CD161 expression on Treg cells was induced by ATRA, which directly regulated the CD161 gene. CD161 was co-stimulatory, and ligation with the T cell antigen receptor induced cytokines that accelerated the wound healing of intestinal epithelial cells. We identified a transcription-factor network, including BACH2, RORγt, FOSL2, AP-1 and RUNX1, that controlled expression of the wound-healing program, and found a CD161+ Treg cell signature in Crohn's disease mucosa associated with reduced inflammation. These findings identify CD161+ Treg cells as a population involved in controlling the balance between inflammation and epithelial barrier healing in the gut