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Research in the Atamas laboratory is focused on the mechanisms of excessive scarring, with emphasis on cellular and molecular interactions between the immune system and connective tissue that lead to abnormal scarring of the lungs. This process, also known as pulmonary fibrosis, occurs in patients with systemic sclerosis (SSc, scleroderma), idiopathic pulmonary fibrosis (IPF), and rheumatoid arthritis (RA). Inflammation and immune activation directly contribute to fibrosis, but, even more importantly, identical cytokines, cell surface molecules, and intracellular signaling pathways appear to be shared between inflammation, immune activation, and scarring. Dr. Atamas’ investigation of these mechanisms is based on a three-pronged approach: research in patients with pulmonary fibrosis, studies in advanced animal models of lung fibrosis, and molecular research in cell culture. The goal of the work is to better understand disease mechanisms at the molecular level and thus form the basis for development of innovative therapies.
Inflammation, Fibrosis, Scleroderma, Systemic Sclerosis, SSc, Idiopathic Pulmonary Fibrosis, IPF, Interstitial Lung Disease, ILD, Cytokines, Chemokines, Cell surface molecules, Lung, Pulmonary, Fibroblasts, T lymphocytes, Macrophages, Animal Models