Abstract

The purpose of this program is to train young physicians or basic scientists for research and teaching careers in rheumatology and thus contribute to the continuing availability of investigators of rheumatic diseases. Persons with an MD degree who have completed their training in internal medicine or in pediatrics and persons with a PhD degree in immunobiology will be considered for the proposed program, provided they have a commitment to an academic career and research in rheumatology. All trainees will be provided with theoretical and practical experience in biomedical research related to rheumatic diseases. The principal method of training will be by participation in research relevant to furthering knowledge in rheumatic diseases. The trainees will participate in seminars, attend lectures and take selected courses to further their theoretical knowledge. The trainees with MD degrees will gain expertise in the diagnosis and treatment of rheumatic diseases to provide them with teaching abilities in this field and to focus their evolving research expertise on rheumatic diseases. These individuals will devote 80% of their time to research training and research. The major areas of research training will be related to immunobiology of rheumatic diseases. Research preceptors will be members of the Division of Rheumatology, Division of Immunology-Rheumatology in Department of Pediatrics, Department of Immunology or members of the Training Program in Molecular Biology. The training facilities consist of the research laboratories of the Division of Rheumatology, Pediatric Rheumatology and the laboratories of other participating faculty members. The outstanding research milieu of the University of Washington is an important factor in the overall research training milieu. The period of training will be three years. Upon completion of this training program, career options include academic appointments in schools of medicine for research or research and teaching in rheumatology. Five postdoctoral positions are requested per year, one being designated for Pediatric Rheumatology.

  Funding Agency

Agency
National Institute of Health (NIH)
Institute
National Institute of Arthritis and Musculoskeletal and Skin Diseases (NIAMS)
Type
Institutional National Research Service Award (T32)
Project #
5T32AR007108-25
Application #
2909743
Study Section
Arthritis and Musculoskeletal and Skin Diseases Special Grants Review Committee (AMS)
Program Officer
Tyree, Bernadette
Project Start
1975-07-01
Project End
2001-06-30
Budget Start
1999-05-01
Budget End
2001-06-30
Support Year
25
Fiscal Year
1999
Total Cost
Indirect Cost

  Institution

Name
University of Washington
Department
Internal Medicine/Medicine
Type
Schools of Medicine
DUNS #
135646524
City
Seattle
State
WA
Country
United States
Zip Code
98195

  Publications

Dam, Elizabeth M; Maier, Alison C; Hocking, Anne M et al. (2018) Increased Binding of Specificity Protein 1 to the IL21R Promoter in B Cells Results in Enhanced B Cell Responses in Rheumatoid Arthritis. Front Immunol 9:1978
Gorman, Jacquelyn A; Hundhausen, Christian; Errett, John S et al. (2017) The A946T variant of the RNA sensor IFIH1 mediates an interferon program that limits viral infection but increases the risk for autoimmunity. Nat Immunol 18:744-752
Sontheimer, Clayton; Liggitt, Denny; Elkon, Keith B (2017) Ultraviolet B Irradiation Causes Stimulator of Interferon Genes-Dependent Production of Protective Type I Interferon in Mouse Skin by Recruited Inflammatory Monocytes. Arthritis Rheumatol 69:826-836
Jackson, Shaun W; Jacobs, Holly M; Arkatkar, Tanvi et al. (2016) B cell IFN-? receptor signaling promotes autoimmune germinal centers via cell-intrinsic induction of BCL-6. J Exp Med 213:733-50
Gazitt, Tal; Lood, Christian; Elkon, Keith B (2016) Citrullination in Rheumatoid Arthritis-A Process Promoted by Neutrophil Lysis? Rambam Maimonides Med J 7:
Buechler, Matthew B; Akilesh, Holly M; Hamerman, Jessica A (2016) Cutting Edge: Direct Sensing of TLR7 Ligands and Type I IFN by the Common Myeloid Progenitor Promotes mTOR/PI3K-Dependent Emergency Myelopoiesis. J Immunol 197:2577-82
Dam, Elizabeth M; Habib, Tania; Chen, Janice et al. (2016) The BANK1 SLE-risk variants are associated with alterations in peripheral B cell signaling and development in humans. Clin Immunol 173:171-180
Shenoi, Susan; Bell, Samantha; Wallace, Carol A et al. (2015) Juvenile idiopathic arthritis in relation to maternal prenatal smoking. Arthritis Care Res (Hoboken) 67:725-30
Elkon, Keith B; Sontheimer, Clayton (2014) Editorial: toll-like receptor 7: more than skin deep? Arthritis Rheumatol 66:481-4
Jackson, Shaun W; Scharping, Nicole E; Kolhatkar, Nikita S et al. (2014) Opposing impact of B cell-intrinsic TLR7 and TLR9 signals on autoantibody repertoire and systemic inflammation. J Immunol 192:4525-32

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