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- Division Overview
- Systemic Autoimmune Diseases Biology Program
- Rheumatic Diseases Genetics and Translational Research Program
- Arthritis Biology Program
- Rheumatic Diseases Clinical Program
- Rheumatic Diseases Biopsychosocial Research Program (includes PROMIS, FMS)
- Extracellular Matrix (ECM) Biology and Diseases Program
- Keratinocyte Biology and Diseases Program
- Immunobiology and Immune Diseases of Skin Program
- Skin Repair, Regeneration and Pigmentation Program
Arthritis Biology Program
Updated March 12, 2012
Arthritis can be caused by diverse processes, such as inflammation, cartilage degeneration, crystal deposition, infection and trauma. The Arthritis Biology program covers basic research in a number of arthritic diseases, including rheumatoid arthritis (RA), juvenile idiopathic arthritis (JIA), Lyme arthritis, viral arthritis, gout, calcium pyrophosphate deposition disease (CPDD), and spondyloarthropathies. The program supports studies of the biology, biochemistry and molecular biology of the synovium, cartilage, and bone and their involvement in disease initiation and perpetuation; studies of lymphoid and inflammatory mediators in pre-clinical and disease onset, analysis of disease triggers and mechanisms in existing and new animal models of disease; studies of manipulation of the immune and inflammatory responses to ameliorate or prevent diseases; the development of imaging and other experimental diagnostic modalities, and new therapeutic modalities in animal models of diseases. The mission of the program is to better understand the molecular mechanisms underlying disease pathogenesis, with the goal of developing treatments and improving patient outcomes.
The following are supported research areas:
- Study the role of components of the innate and adaptive immune systems, and associated signaling pathways, on the initiation and propagation of arthritis.
- Study the involvement and the cross-talk of a wide range of hematopoietic and other cell types in arthritis.
- Explore joint tissue remodeling pathways to better understand the mechanisms of tissue damage, and to identify new therapeutic targets.
- Study the contribution of dysregulated cellular processes (e.g., programmed cell death, necrosis, autophagy) to the etiology and pathogenesis of arthritis.
- Develop animal models to study the immune and inflammatory mechanisms of arthritis, as well as the pathogenic pathways identified by GWAS and other human genetics research.
- Couple animal models with systems biology approaches, to identify critical cellular and molecular pathways involved in pathogenesis, and to facilitate identification of therapeutic targets.
- Investigate comorbidities of arthritis using animal models to dissect mechanisms of extra-articular organ involvement.
- Investigate the use of non-invasive imaging technologies in functional studies of disease prognosis and disease course.
Su-Yau Mao, Ph.D.
Arthritis Biology Program
Division of Skin and Rheumatic Diseases
NIAMS, NIH, DHHS
One Democracy Plaza
6701 Democracy Blvd., Ste. 800
Bethesda, MD 20892-4872