Dana P. Ascherman, M.D.
Call 305-243-4000 or request an appointment online
- Fax: 305-243-7546
- Rheumatology-Internal Medicine
- Internal Medicine
Dr. Ascherman’s clinical practice encompasses a range of systemic autoimmune diseases, with a particular focus on idiopathic inflammatory myopathy (polymyositis/dermatomyositis, inclusion body myositis). These clinical interests dovetail with Dr. Ascherman’s basic and translational research program that also includes investigation of the overlap between autoimmune disorders and interstitial lung diseases (ILD). As part of the latter effort, Dr. Ascherman co-founded the interdisciplinary Autoimmune Interstitial Lung Disease Clinic which he directs with Dr. Marilyn Glassberg (Pulmonary Medicine).
- American Board of Internal Med-Rheumatology
- Associate Professor of Medicine
Dr. Ascherman’s research centers on the role of cell-mediated immunity in the pathogenesis of idiopathic inflammatory myopathy, a systemic autoimmune disorder resulting in damage to muscle as well as extra-muscular tissues that include skin, joints, lung, and the vascular system. While this effort initially focused on human cells and tissue, the relative rarity of this disorder led Dr. Ascherman to develop a novel antigen-induced model replicating several cardinal features of this disease—namely, myositis and interstitial lung disease (ILD). Beyond support for the role of histidyl-tRNA synthetase (HRS=Jo-1) in human disease, this work has generated some intriguing observations regarding the ability of peptides to generate species-specific antibody responses--fueling a computational biology collaboration investigating the contribution of peptide stability to antigenicity, immunogenicity, and affinity maturation. Complementing these studies, more recent work has explored the interaction between HRS and signaling components of the innate immune system that not only support the development of class-switched autoantibody responses, but also promote a robust myositis phenotype. Dissecting the relationship between HRS-induced innate immune activation, NF-kB-mediated transcriptional pathways, and muscle dysfunction therefore represents a major ongoing research effort. At the same time, the connection between myositis and inflammatory lung disease in humans has fueled more translational studies focusing on biomarker discovery in connective tissue disease-associated ILD. Collectively, these efforts underscore an expanding basic and translational research program uniting themes of autoimmune disease mechanisms and structural immunology.
- Anti-Citrullinated Heat Shock Protein 90 Antibodies Isolated from Bronchoalveolar Lavage Fluid are a Marker of Lung-Specific Immune Responses,
- Biomarkers of Rheumatoid Arthritis-associated Interstitial Lung Disease
- Identification of Citrullinated Heat Shock Protein 90 Isoforms as Novel Autoantigens in Rheumatoid Arthritis-associated Interstitial Lung Disease
- Functional Redundancy of MyD88-dependent Signaling Pathways in a Murine Model of Histidyl-tRNA Synthetase-induced Myositis