David E. Justus
University of Louisville
22 Papers
273 Citations
David E. Justus is an academic researcher from University of Louisville. The author has contributed to research in topics: Complement control protein & Complement system. The author has an hindex of 13, co-authored 22 publications.
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Papers
The inflammation modulatory protein (IMP) of cowpox virus drastically diminishes the tissue damage by down-regulating cellular infiltration resulting from complement activation.
TL;DR: The function of IMP in vivo in mice with a complete repertoire of immune components is to limit cellular infiltration by down regulating the complement derived chemotactic analphylotoxins, thereby modulating the inflammatory response contributing to a diminished tissue pathology and preservation of viral habitat.
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Molecular mimicry of the inflammation modulatory proteins (IMPs) of poxviruses: evasion of the inflammatory response to preserve viral habitat
TL;DR: Evidence for molecular mimicry and evolutionary relationship to other homologs of IMP is presented and their relationships with other IMPs such as the poxviral chemokine and cytokine receptor‐like proteins are discussed.
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Outer membrane vesicles of Porphyromonas gingivalis inhibit IFN-γ-mediated MHC class II expression by human vascular endothelial cells
TL;DR: In this article, outer membrane vesicles were isolated from cultures of Porphyromonas gingivalis and tested for their ability to promote inflammation and for their effects on the biosynthesis of E-selectin and ICAM-1 adhesion molecules and MHC class II glycoproteins.
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Severe and prolonged inflammatory response to localized cowpox virus infection in footpads of C5-deficient mice: investigation of the role of host complement in poxvirus pathogenesis.
TL;DR: There is a significant variation in the primary response in the two different mouse strains to cowpox virus infection, which strongly suggests that the host complement plays a significant role during the initial response to poxvirus infection.
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Immunosuppression in malaria: effect of hemozoin produced by Plasmodium berghei and Plasmodium falciparum.
Nimit Morakote,David E. Justus +1 more
TL;DR: The results of the present study strongly suggest that the inhibition of macrophage accessory cell activity is due, at least in part, to the uptake and accumulation of hemozoin in their cytoplasms.
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