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InnateDB: systems biology of innate immunity and beyond—recent updates and continuing curation

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TLDR
The recent integration of bovine data makes InnateDB the first integrated network analysis platform for this agriculturally important model organism, and a range of improvements to the integrated bioinformatics solutions are reported.
Abstract
InnateDB (http://www.innatedb.com) is an integrated analysis platform that has been specifically designed to facilitate systems-level analyses of mammalian innate immunity networks, pathways and genes. In this article, we provide details of recent updates and improvements to the database. InnateDB now contains >196 000 human, mouse and bovine experimentally validated molecular interactions and 3000 pathway annotations of relevance to all mammalian cellular systems (i.e. not just immune relevant pathways and interactions). In addition, the InnateDB team has, to date, manually curated in excess of 18 000 molecular interactions of relevance to innate immunity, providing unprecedented insight into innate immunity networks, pathways and their component molecules. More recently, InnateDB has also initiated the curation of allergy- and asthma-related interactions. Furthermore, we report a range of improvements to our integrated bioinformatics solutions including web service access to InnateDB interaction data using Proteomics Standards Initiative Common Query Interface, enhanced Gene Ontology analysis for innate immunity, and the availability of new network visualizations tools. Finally, the recent integration of bovine data makes InnateDB the first integrated network analysis platform for this agriculturally important model organism.

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References
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A cytokine-mediated link between innate immunity, inflammation, and cancer

TL;DR: An overview of the current understanding of the role of inflammation-induced cytokines in tumor initiation, promotion, and progression is provided.
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Innate immunity and intestinal microbiota in the development of Type 1 diabetes

TL;DR: It is found that MyD88 deficiency changes the composition of the distal gut microbiota, and that exposure to the microbiota of specific pathogen-free MyD 88-negative NOD donors attenuates T1D in germ-free NOD recipients.
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