Abstract
Recent thymic emigrants are the youngest subset of peripheral T cells and their involvement in combating persistent bacterial infections has not been explored. Here, we hypothesized that CD4+ recent thymic emigrants are essential immune mediators during persistent Salmonella infection. To test this, we thymectomized adult mice either prior to, or during, persistent Salmonella infection. We found that thymic output is crucial in the formation of protective immune responses during the early formation of a Salmonella infection but is dispensable once persistent Salmonella infection is established. Further, we show that thymectomized mice demonstrate increased infection-associated mortality and bacterial burdens. Unexpectedly, numbers of Salmonella-specific CD4+ T cells were significantly increased in thymectomized mice compared to sham control mice. Lastly, we found that T cells from thymectomized mice may be impaired in producing the effector cytokine IL-17 at early time points of infection, compared to thymically intact mice. Together, these results imply a unique role for thymic output in the formation of immune responses against a persistent, enteric pathogen.
Highlights
The thymus serves as the anatomical site where new cytotoxic (CD8+ ) and helper (CD4+ ) T cells initially express the T cell receptor (TCR)
What is not known is whether existing peripheral CD4 T cells are sufficient to control infection or whether a continuous supply of new T cells is important for controlling bacterial infection
We sought to determine the impact of thymic output on the establishment of a persistent Salmonella infection by thymectomizing resistant mice and assessing the impact of the lack of a thymus on infection
Summary
The thymus serves as the anatomical site where new cytotoxic (CD8+ ) and helper (CD4+ ) T cells initially express the T cell receptor (TCR). Much of the impact of infection on the thymus has been attributed to increased systemic levels of glucocorticoids (GC) and pro-inflammatory cytokines, which have a negative impact on thymopoiesis and induce acute thymic atrophy. Many of these outcomes are temporary and are generally resolved upon cessation of the immunological stress [6]
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