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Robin G. Lorenz

Researcher at University of Alabama at Birmingham

Publications -  113
Citations -  7117

Robin G. Lorenz is an academic researcher from University of Alabama at Birmingham. The author has contributed to research in topics: Immune system & T cell. The author has an hindex of 40, co-authored 106 publications receiving 6687 citations. Previous affiliations of Robin G. Lorenz include University of Washington & Medical University of South Carolina.

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Interleukin 17-producing T helper cells and interleukin 17 orchestrate autoreactive germinal center development in autoimmune BXD2 mice.

TL;DR: It is demonstrated that autoimmune BXD2 mice express more IL-17 and show spontaneous development of germinal centers (GCs) before they increase production of pathogenic autoantibodies, suggesting a mechanism by which IL- 17 drives autoimmune responses by promoting the formation of spontaneous GCs.
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Experimental Models of Inflammatory Bowel Disease Reveal Innate, Adaptive, and Regulatory Mechanisms of Host Dialogue With the Microbiota

TL;DR: The thesis is advanced that ‘multiple hits’ or defects in these interacting components is required for IBD to occur in both mouse and human.
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The gastrointestinal ecosystem: a precarious alliance among epithelium, immunity and microbiota.

TL;DR: The gastrointestinal (GI) tract is a complex ecosystem generated by the alliance of GI epithelium, immune cells and resident microbiota that can result in a broken alliance and subsequent GI pathology.
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Epithelial attachment alters the outcome of Helicobacter pylori infection

TL;DR: The impact of attachment on the course of infection was examined in transgenic mice expressing a human receptor for H. pylori in their gastric epithelium and this model should help identify bacterial and host genes that produce attachment-related pathology.
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Cyclooxygenase-2-dependent arachidonic acid metabolites are essential modulators of the intestinal immune response to dietary antigen.

TL;DR: It is established that cyclooxygenase-2-dependent arachidonic acid metabolites are essential in the development and maintenance of intestinal immune homeostasis.