Abstract
Abstract Our current understanding of effector cell differentiation suggests that inflammation plays an important role in driving an activated cell down the short lived effector cell (SLEC) versus memory precursor effector cell (MPEC) pathway. While IL-12 has been implicated as an important regulator of differentiation, this appears not to be the case for all infections, e.g. vaccinia virus (VV). To evaluate factors that may regulate effector cell differentiation under these circumstances, we investigated the effect of viral dose. We found that mice infected with a low dose of vaccinia virus had more B8R-specific cells at the peak of the response compared to those infected with a high dose of virus. Surprisingly, the observed increase in total number was the result of an increased SLEC population, leading to a response skewed toward SLEC. The increased SLEC in the low dose infected mice was not due to selective increases in proliferation or decreases in death (as measured by active caspase 3) in this population. In exploring this model we found that T regulatory cells were present at higher numbers in high dose infected mice. However, while depletion of Tregs led to an increase in the number of B8R specific cells, it did not result in a selective increase in SLEC. These data support a role for viral burden in effector cell differentiation, with decreased vaccinia virus dose driving the formation of SLEC.
Published Version
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call