The Immunology of Type 1 Diabetes Core provides logistic support to investigators examining autoimmune or type 1 diabetes or other endocrine autoimmunities. The Core is centered in the Department of Pathology and Immunology. The Core provides: i) assistance in the maintenance of various inbred mouse lines, including conventional non-obese diabetic (NOD) mice and NOD lines in which a variety of immune-relevant molecules has been deleted;ii) training in the maintenance and testing of diabetogenic strains;iii) expertise in, and training for, the isolation and examination of islets of Langerhans;iv) services for the generation of new diabetogenic mouse strains using Balb/c and NOD embryonic stem cells;and v) provision of isolated cells, cell lines, and monoclonal antibodies relevant for immunological research. During the past funding cycle, services were provided to 31 investigators, which represents a doubling of service provided compared to the prior funding cycle. This reflects, in part, increased utilization of the most frequently requested service, maintenance and provision of inbred strains. The increase also reflects the new services for provision of cell lines, isolated immune cells, antibodies and peptides. The Core provides service to and has helped to cultivate a diverse group of investigators at Washington University with a commitment to studying the pathogenesis and treatment of type 1 diabetes. Services from this Core were instrumental in facilitating high impact studies of the immunobiology of type 1 diabetes.
The Core provides services to facilitate the investigations of immunologists and diabetologists working to understand the pathogenesis of type 1 diabetes. The Core services are particulariy useful to faculty starting their own laboratories, or to faculty wishing to carry out pilot studies using autoimmune propensity mice. Importantly, this Core provides assistance with highly specialized immune models of type 1 diabetes that can be difficult to generate and propagate.
|Rusconi, B; Jiang, X; Sidhu, R et al. (2018) Gut Sphingolipid Composition as a Prelude to Necrotizing Enterocolitis. Sci Rep 8:10984|
|Chen, Yana; McCommis, Kyle S; Ferguson, Daniel et al. (2018) Inhibition of the Mitochondrial Pyruvate Carrier by Tolylfluanid. Endocrinology 159:609-621|
|Zhang, Yan; Rohatgi, Nidhi; Veis, Deborah J et al. (2018) PGC1? Organizes the Osteoclast Cytoskeleton by Mitochondrial Biogenesis and Activation. J Bone Miner Res 33:1114-1125|
|Xu, Wei; Mukherjee, Sumit; Ning, Yu et al. (2018) Cyclopropane fatty acid synthesis affects cell shape and acid resistance in Leishmania mexicana. Int J Parasitol 48:245-256|
|Hughes, Jing W; Bao, Yicheng K; Salam, Maamoun et al. (2018) Late-Onset T1DM and Older Age Predict Risk of Additional Autoimmune Disease. Diabetes Care :|
|Zhang, Xiangyu; Evans, Trent D; Jeong, Se-Jin et al. (2018) Classical and alternative roles for autophagy in lipid metabolism. Curr Opin Lipidol 29:203-211|
|Ban, Norimitsu; Lee, Tae Jun; Sene, Abdoulaye et al. (2018) Disrupted cholesterol metabolism promotes age-related photoreceptor neurodegeneration. J Lipid Res 59:1414-1423|
|Ban, Norimitsu; Lee, Tae Jun; Sene, Abdoulaye et al. (2018) Impaired monocyte cholesterol clearance initiates age-related retinal degeneration and vision loss. JCI Insight 3:|
|Mayer, Allyson L; Zhang, Yiming; Feng, Emily H et al. (2018) Enhanced Hepatic PPAR? Activity Links GLUT8 Deficiency to Augmented Peripheral Fasting Responses in Male Mice. Endocrinology 159:2110-2126|
|Weber, Kassandra J; Sauer, Madeline; He, Li et al. (2018) PPAR? Deficiency Suppresses the Release of IL-1? and IL-1? in Macrophages via a Type 1 IFN-Dependent Mechanism. J Immunol 201:2054-2069|
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