The over-arching mission of the Animal Models of inflammatory Disease Core is to support investigators of the Cincinnati Children's Hospital Research Community in the use of experimental animal settings of rheumatic diseases, autoimmune diseases, and inflammatory processes. In so doing, the Core will promote advances in the understanding and treatment of arthritic and auto-inflammatory diseases. Animal models, particularly those involving murine systems, have emerged as powerful tools in arthritis and autoimmune research due to the fact that any gene identified as a candidate """"""""disease modifier"""""""" can be easily manipulated in mice through either """"""""gene-targeting"""""""" or standard transgenic technologies. In providing an in vivo experimental system amenable to investigator-imposed genetic alterations (e.g., loss-of-function or gain-of function), animal models offer the unique opportunity (not available in human subjects) to test hypotheses focused on identifying the fundamental mechanisms that drive auto-inflammatory disease. Animal models offer the ability of collecting entire tissues (i.e., whole joints) for detailed analyses of biochemical, immunological, pathological and gene expression properties, and as well as performing comprehensive temporal analyses of disease progression. The utility of animal models has been highlighted by the fact that these experimental systems have often provided the early proof-of-principle for some of the most powerful therapeutic strategies (e.g., anti-cytokine therapies such as TNF blockers). Finally, many animal models of arthritis and other auto-inflammatory diseases are available with distinct etiologies (e.g., adaptive immune driven vs. cytokine driven), and thus provide a variety of distinct frameworks to study these complex disease processes.
The Specific Aims of the Animal Models of Inflammatory Diseases Core are to (i) provide technical expertise and starter reagents to investigators interested in animal models of auto-inflammatory disease (i.e., arthritis, neuroinflammatory disease, and dermatomyositis), and (ii) provide material assistance in the generation and characterization of both transgenic and gene-targeted mice that will be instructive with regard to the development and progression of auto-inflammatory disease. This core serves as the perfect complement to ongoing basic and clinical studies (e.g., immunology, informatics, and gene discovery) of the Cincinnati Rheumatic Diseases Core Center Research Base.

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Center Core Grants (P30)
Project #
5P30AR047363-12
Application #
8381259
Study Section
Special Emphasis Panel (ZAR1-MLB)
Project Start
Project End
Budget Start
2012-07-01
Budget End
2013-06-30
Support Year
12
Fiscal Year
2012
Total Cost
$123,438
Indirect Cost
$43,301
Name
Cincinnati Children's Hospital Medical Center
Department
Type
DUNS #
071284913
City
Cincinnati
State
OH
Country
United States
Zip Code
45229
McNally, Jonathan P; Millen, Scott H; Chaturvedi, Vandana et al. (2017) Manipulating DNA damage-response signaling for the treatment of immune-mediated diseases. Proc Natl Acad Sci U S A 114:E4782-E4791
Hinks, A; Bowes, J; Cobb, J et al. (2017) Fine-mapping the MHC locus in juvenile idiopathic arthritis (JIA) reveals genetic heterogeneity corresponding to distinct adult inflammatory arthritic diseases. Ann Rheum Dis 76:765-772
Chimote, Ameet A; Hajdu, Peter; Sfyris, Alexandros M et al. (2017) Kv1.3 Channels Mark Functionally Competent CD8+ Tumor-Infiltrating Lymphocytes in Head and Neck Cancer. Cancer Res 77:53-61
Feldhoff, Lea M; Rueda, Cesar M; Moreno-Fernandez, Maria E et al. (2017) IL-1? induced HIF-1? inhibits the differentiation of human FOXP3+ T cells. Sci Rep 7:465
McKnight, Christopher G; Jude, Joseph A; Zhu, Zhenqi et al. (2017) House Dust Mite-Induced Allergic Airway Disease Is Independent of IgE and Fc?RI?. Am J Respir Cell Mol Biol 57:674-682
Ombrello, Michael J; Arthur, Victoria L; Remmers, Elaine F et al. (2017) Genetic architecture distinguishes systemic juvenile idiopathic arthritis from other forms of juvenile idiopathic arthritis: clinical and therapeutic implications. Ann Rheum Dis 76:906-913
Smith, Eric A; Gole, Boris; Willis, Nicholas A et al. (2017) DEK is required for homologous recombination repair of DNA breaks. Sci Rep 7:44662
Lo, Yuan-Hung; Chung, Eunah; Li, Zhaohui et al. (2017) Transcriptional Regulation by ATOH1 and its Target SPDEF in the Intestine. Cell Mol Gastroenterol Hepatol 3:51-71
Thornton, Sherry; Raghu, Harini; Cruz, Carolina et al. (2017) Urokinase plasminogen activator and receptor promote collagen-induced arthritis through expression in hematopoietic cells. Blood Adv 1:545-556
Rueda, Cesar M; Rodríguez-Perea, Ana Lucia; Moreno-Fernandez, Maria et al. (2017) High density lipoproteins selectively promote the survival of human regulatory T cells. J Lipid Res 58:1514-1523

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