D
David S. Ucker
Researcher at University of Illinois at Chicago
Publications - 49
Citations - 4863
David S. Ucker is an academic researcher from University of Illinois at Chicago. The author has contributed to research in topics: Innate immune system & Apoptosis. The author has an hindex of 25, co-authored 48 publications receiving 4645 citations.
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Journal ArticleDOI
Mesenchymal stem cells suppress lymphocyte proliferation in vitro and prolong skin graft survival in vivo.
Amelia Bartholomew,Cord Sturgeon,Mandy Siatskas,Karen Ferrer,Kevin R. Mcintosh,Sheila Patil,Wayne Hardy,S. Devine,David S. Ucker,Robert J. Deans,Annemarie Moseley,Ronald Hoffman +11 more
TL;DR: Baboon MSCs have been observed to alter lymphocyte reactivity to allogeneic target cells and tissues, which may prove useful in future applications of tissue regeneration and stem cell engineering.
Journal Article
Chemopreventive Isothiocyanates Induce Apoptosis and Caspase-3-like Protease Activity
TL;DR: The results suggest that isothiocyanates may induce apoptosis through a caspase-3-dependent mechanism, and may provide a distinct mechanism for their chemopreventive functions.
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Distinct modes of macrophage recognition for apoptotic and necrotic cells are not specified exclusively by phosphatidylserine exposure.
Regina E. Cocco,David S. Ucker +1 more
TL;DR: Using objective and quantitative measures, it is found that macrophages bind and engulf native apoptotic and necrotic cells to similar extents and with similar kinetics, however, recognition of these two classes of dying cells occurs via distinct and noncompeting mechanisms.
Journal Article
Activation-driven T cell death. I. Requirements for de novo transcription and translation and association with genome fragmentation.
TL;DR: It is hypothesized that activation-driven cell death may be involved in vivo in the clonal deletion of auto-reactive T cells during T cell ontogeny.
Journal ArticleDOI
Innate immune discrimination of apoptotic cells: repression of proinflammatory macrophage transcription is coupled directly to specific recognition.
Marija Cvetanovic,David S. Ucker +1 more
TL;DR: The data demonstrate that apoptotic cells target the proinflammatory transcriptional machinery of macrophages with which they interact, without apparent effect on proximal steps of Toll-like receptor signaling.