Emergency BU Alert BU Medical Campus OPEN Jan. 28, 2015 Boston University Medical Campus will be open Wednesday, Jan. 28, 2015. BUSM classes will be held as scheduled. Staff should check with their managers regarding work schedules. Medical, PA and GMS students who are assigned to inpatient services or clinics are expected to be present, if possible. Students who are assigned to outpatient services should check with their course director or the policy at the clinical site. GMS classes are canceled. Staff should check with their manager regarding their work schedules. The Henry M. Goldman School of Dental Medicine will follow normal school hours. All Patient Treatment Centers will be open for patient care and all classes will be held as scheduled. BU School of Public Health classes are canceled; SPH non-essential staff may telecommute. Employees who are part of the BUMC parking program should park in your assigned lot or garage. The Boston parking ban is still in effect. For updated information, please call the weather/emergency hotline at 617-638-6886 or visit the BU Emergency Communications website at http://www.bu.edu/ehs/comm/

Robert Lafyatis M.D.

Medicine-Rheumatology

Office: 715 Albany St, E
Phone: 617-638-4310
Email: lafyatis@bu.edu

Research:

Dr. Lafyatis carries out patient oriented research into the cause and treatment of systemic sclerosis. This includes early phase clinical trials into new therapeutic agents in patients with systemic sclerosis. He has been investigating the mechanisms of actions and markers of response for novel therapeutics, such as the B cell depleting agent, rituximab and the immunosuppressant agent, mycophenlate. Additional studies are aimed at identifying biomarkers in systemic sclerosis using microarray gene expression analysis of skin and blood in scleroderma patients. Ongoing biomarker studies include investigation into molecular markers of pulmonary hypertension in systemic sclerosis. Dr. Lafyatis also carries out basic research into the cause of fibrosis and vasculopathy in systemic sclerosis using patient samples and murine disease models. His studies have provided key insights into one widely used model of systemic sclerosis, the tight skin mouse. His studies are currently focused on understanding how autoimmunity and the innate immune system lead to fibrosis and vascular damage. This has recently led to the discovery of increased interferon-regulated gene expression in white blood cells of patients with systemic sclerosis. Ongoing research is aimed at better understanding the cause of altered gene expression by monocytes and other cells in the innate immune system.

Affiliated Websites:

Immunology Training Program Webpage