Figure 1
Skin epidermal infection by virus leads to TRM residency and local or global antiviral protection. When the host is infected via skin scarification, the resulting inflammation increases expression of chemoattractants and adhesion molecules such as P- and E-selectin on the endothelium of the blood vessels. T cells activated through this route upregulate skin homing markers such as P- and E-selectin ligands. Collectively, these events lead to the recruitment of circulating, antigen-specific effector/effector memory (TEM) CD8 T cells into the infected tissue. The recruited CD8 T cells establish a pool of resident memory T cells (TRM) that can provide protection against future skin infections. Jiang et al. show that upon multiple skin immunizations, circulating effector/TEM CD8 T cells also accumulate at uninfected sites. These CD8 T cells can then form a TRM population that is immunologically protective. However, the establishment of TRM in uninfected skin is dependent on the route of immunization, as skin-independent methods such as intraperitoneal injection did not lead to protection against a secondary skin challenge.
