Rheumatologists are experts in treating arthritis and autoimmune diseases. Rheumatologists are specially trained to diagnose and treat inflammatory diseases of the joints and soft tissues (tendons, ligaments, muscles, and bones), and care for patients with arthritis, gout, tendonitis and a variety of other joint and connective tissue disorders.
Inflammation of the joints, muscles and other soft tissues are caused by wear and tear, infection, or disorders of the immune system, called autoimmune diseases. These latter conditions include rheumatoid arthritis, lupus, polymyositis, polymyalgia rheumatica, and many forms of vasculitis. Recent advancements in understanding the causes of arthritis led to the introduction of new medications that revolutionized the treatment of many debilitating joint diseases.
Application of cytokine-blocking therapy to systemic rheumatic diseases
Cytokine-signaling pathways that regulate Treg development and function in SLE
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Lupus is a disease in which a person’s immune system attacks and destroys his/her own cells. This leads to chronic inflammation and damage in joints and various organs, such as skin, brain, lungs, heart, and kidneys. Lupus symptoms can be temporarily controlled with medication; however, there is no cure for lupus and many patients die from their illness or side effects from immunosuppressive drugs. Therefore, it is critical to understand what is happening inside the immune system cells of lupus patients to be able to develop target-specific treatments that cause only minimal side effects. A regulatory T (Treg) cell is a type of white blood cell in the immune system which suppresses harmful inflammation in the body. Previous studies suggest that a decrease in the number and/or function of Treg-cell can lead to uncontrolled inflammation in lupus. Therefore, it is possible to develop treatment that effectively restores the lupus Treg population and its function by understanding what controls the number and function of Tregs at the cellular level. I am studying the mechanims underlying the diminished Treg function using blood specimens from lupus patients.