Tissue-resident memory T cells in cytomegalovirus infection.

Herpesviruses establish life-long infection in their hosts and maintain latent reservoirs for sporadic reactivation at peripheral sites, such as skin and mucosae. For herpes simplex virus infection, experimental studies in mice revealed that immediate protection against local reactivation or superinfection events in the skin relies on tissue resident memory T cells (TRM) rather than on their circulating counterparts. Recent evidence extends this notion to cytomegalovirus infection, which potently induces TRM cells in both mice and humans particularly in mucosal tissues that constitute important viral sanctuaries and are relevant entry sites for challenge and superinfections.

The Salivary Gland Acts as a Sink for Tissue-Resident Memory CD8(+) T Cells, Facilitating Protection from Local Cytomegalovirus Infection.

Tissue-resident memory T cells (TRM) reside in barrier tissues and provide local immediate protective immunity. Here, we show that the salivary gland (SG) most-effectively induces CD8(+) and CD4(+) TRM cells against murine cytomegalovirus (MCMV), which persists in and spreads from this organ. TRM generation depended on local antigen for CD4(+), but not CD8(+), TRM cells, highlighting major differences in T cell subset-specific demands for TRM development.