@article{dogra_miller-kittrell_pitt_jackson_masi_copeland_wu_miller_sparer_2016, title={A little cooperation helps murine cytomegalovirus (MCMV) go a long way: MCMV co-infection rescues a chemokine salivary gland defect}, volume={97}, journal={Journal of General Virology}, author={Dogra, P. and Miller-Kittrell, M. and Pitt, E. and Jackson, J. W. and Masi, T. and Copeland, C. and Wu, S. and Miller, W. and Sparer, T.}, year={2016}, pages={2957–2972} }
 @article{crook_miller-kittrell_morrison_scholle_2014, title={Modulation of innate immune signaling by the secreted form of the West Nile virus NS1 glycoprotein}, volume={458}, ISSN={["0042-6822"]}, DOI={10.1016/j.virol.2014.04.036}, abstractNote={West Nile virus (WNV) employs several different strategies to escape the innate immune response. We have previously demonstrated that the WNV NS1 protein interferes with signal transduction from Toll-like receptor 3 (TLR3). NS1 is a glycoprotein that can be found intracellularly or associated with the plasma membrane. In addition, NS1 is secreted to high levels during flavivirus infections. We investigated whether the secreted form of NS1 inhibits innate immune signaling pathways in uninfected cells. Secreted NS1 (sNS1) was purified from supernatants of cells engineered to express the protein. Purified sNS1 associated with and repressed TLR3-induced cytokine production by HeLa cells, and inhibited signaling from TLR3 and other TLRs in bone marrow-derived macrophages and dendritic cells. Footpad administration of sNS1 showed the protein associated predominantly with macrophages and dendritic cells in the draining lymph node. Additionally, sNS1 significantly reduced TLR3 signaling and WNV replicon particle-mediated cytokine transcription in popliteal lymph nodes.}, journal={VIROLOGY}, author={Crook, Kristen R. and Miller-Kittrell, Mindy and Morrison, Clayton R. and Scholle, Frank}, year={2014}, month={Jun}, pages={172–182} }
 @article{winkelmann_widman_xia_ishikawa_miller-kittrell_nelson_bourne_scholle_mason_milligan_2012, title={Intrinsic adjuvanting of a novel single-cycle flavivirus vaccine in the absence of type I interferon receptor signaling}, volume={30}, ISSN={["1873-2518"]}, DOI={10.1016/j.vaccine.2011.12.103}, abstractNote={Type I interferons (IFNs) are critical for controlling pathogenic virus infections and can enhance immune responses. Hence their impact on the effectiveness of live-attenuated vaccines involves a balance between limiting viral antigen expression and enhancing the development of adaptive immune responses. We examined the influence of type I IFNs on these parameters following immunization with RepliVAX WN, a single-cycle flavivirus vaccine (SCFV) against West Nile virus (WNV) disease. RepliVAX WN-immunized mice produced IFN-α and displayed increased IFN-stimulated gene transcription in draining lymph nodes (LN). SCFV gene expression was over 100 fold-higher on days 1-3 post-infection in type I IFN receptor knockout mice (IFNAR(-/-)) compared to wild-type (wt) mice indicating a profound IFN-mediated suppression of SCFV gene expression in the wt animals. IFNAR(-/-) mice produced nearly equivalent levels of WNV-specific serum IgG and WNV-specific CD4(+) T cell responses compared to wt mice. However, significantly higher numbers of WNV-specific CD8(+) T cells were produced by IFNAR(-/-) mice and a significantly greater percentage of these T cells from IFNAR(-/-) mice produced only IFN-γ following antigen-specific re-stimulation. This altered cytokine expression was not associated with increased antigen load suggesting the loss of type I IFN receptor signaling was responsible for the altered quality of the CD8(+) effector T cell response. Together, these results indicate that although type I IFN is not essential for the intrinsic adjuvanting of RepliVAX WN, it plays a role in shaping the cytokine secretion profiles of CD8(+) effector T cells elicited by this SCFV.}, number={8}, journal={VACCINE}, author={Winkelmann, Evandro R. and Widman, Douglas G. and Xia, Jingya and Ishikawa, Tomohiro and Miller-Kittrell, Mindy and Nelson, Michelle H. and Bourne, Nigel and Scholle, Frank and Mason, Peter W. and Milligan, Gregg N.}, year={2012}, month={Feb}, pages={1465–1475} }