@article{85686,
  keywords = {Animals, signal transduction, Cell Proliferation, Mice, Cells, Cultured, Mice, Knockout, CD8-Positive T-Lymphocytes, Dendritic Cells, Immunologic Memory, Interleukin-10, Listeria monocytogenes, Listeriosis, Lymphocyte Activation, Receptors, Interleukin-10},
  author = {Partha Sarathi Biswas and Virginia Pedicord and Alexander Ploss and Ewa Menet and Ingrid Leiner and Eric Pamer},
  title = {Pathogen-specific CD8 T cell responses are directly inhibited by IL-10.},
  abstract = {<p>Regulation of CD8 T cell expansion and contraction is essential for successful immune defense against intracellular pathogens. IL-10 is a regulatory cytokine that can restrict T cell responses by inhibiting APC functions. IL-10, however, can also have direct effects on T cells. Although blockade or genetic deletion of IL-10 enhances T cell-mediated resistance to infections, the extent to which IL-10 limits in vivo APC function or T cell activation/proliferation remains unknown. Herein, we demonstrate that primary and memory CD8 T cell responses following Listeria monocytogenes infection are enhanced by the absence of IL-10. Surface expression of the IL-10R is transiently up-regulated on CD8 T cells following activation, suggesting that activated T cells can respond to IL-10 directly. Consistent with this notion, CD8 T cells lacking IL-10R2 underwent greater expansion than wild-type T cells upon L. monocytogenes infection. The absence of IL-10R2 on APCs, in contrast, did not enhance T cell responses following infection. Our studies demonstrate that IL-10 produced during bacterial infection directly limits expansion of pathogen-specific CD8 T cells and reveal an extrinsic regulatory mechanism that modulates the magnitude of memory T cell responses.</p>
},
  year = {2007},
  journal = {J Immunol},
  volume = {179},
  pages = {4520-8},
  month = {10/2007},
  issn = {0022-1767},
  language = {eng},
}