Optimization of TCR transgenic T cells for in vivo tracking of immune responses.

T-cell receptor (TCR) transgenic mice have proven useful for the study of various immune parameters. Despite this, it has been suggested that transferred T cells respond differently to their endogenous counterparts at least in terms of conversion to antigen-experienced populations bearing memory cell markers. Here, we have compared the response of TCR transgenic T cells to endogenous populations within the context of infection with herpes simplex virus.

Latent infection with herpes simplex virus is associated with ongoing CD8+ T-cell stimulation by parenchymal cells within sensory ganglia.

CD8+ T-cell persistence can be seen in ganglia harboring latent herpes simplex virus (HSV) infection. While there is some evidence that these cells suppress virus reactivation, this view remains controversial. Given that maintenance of latency by CD8+ T cells would necessitate ongoing exposure to antigen within this site, we sought evidence for such chronic stimulation.

Distinct migrating and nonmigrating dendritic cell populations are involved in MHC class I-restricted antigen presentation after lung infection with virus.

During lung infection with virus, airway-derived dendritic cells (DC) have been thought to be the dominant cell type involved in acquisition, transport, and direct antigen presentation for cytotoxic T lymphocyte priming. Contrary to this view, we have found that both an airway-derived CD8alpha(-)CD11b(-) DC subset and distinct CD8alpha(+) lymph node resident DC can present class I-restricted antigens after lung infection with influenza virus or herpes simplex virus 1. Presentation by a nonairway-derived DC population argues that cytotoxic T lymphocyte priming may involve interplay between different DC subsets, not all of which originate within the site of infection.