Michael York MD

Assistant Professor

Education:

MD, University of Massachusetts

General field of research:

Scleroderma; Autoimmunity.

Affiliations other than medicine:

Evans Center for Interdisciplinary Biomedical Research

Contact information:

Office
72 East Concord St. Evans 501 Arthritis Center

Phone: (617)-638 4524

Fax: (617)-638 5226

mikyork@bu.edu

Other research websites:

http://www.bumc.bu.edu/rheumatology/scleroderma/

Research group information:

Cindy Collins, Research Assistant

Keywords:

Scleroderma; Raynaud’s Phenomenon; Toll-like receptors; Pulmonary Hypertension.

Summary of research interest:

Our group is currently investigating the role of the innate immune system on the development of systemic sclerosis (scleroderma). This disease is characterized by thick skin and scarring of internal organs such as the lungs as well as vascular problems such as Raynaud’s phenomenon, pulmonary hypertension and gangrene. We are trying to determine how the immune system causes these problems and develop new therapeutics to treat this disease.

We are currently focusing on how dysfunction of the patient’s immune system occurs and how this leads to vascular and fibrotic disease. We are focusing on receptors of the innate immune system called toll-like receptors that typically recognize viral or bacterial DNA or RNA. Recently it has been found that immune complexes found in patients with Systemic Lupus Erythematosus or Scleroderma can trigger these receptors by allowing self-DNA or RNA to enter cells, thereby overcoming some of the protective mechanisms preventing the host to develop an immune response against itself.

york_lab-photo

Recent publications:

Lafyatis R, Kissin E, York M, Farina G, Viger K, Fritzler MJ, Merkel PA and Simms RW. 2009.  B Cell depletion with rituximab in patients with diffuse cutaneous systemic sclerosis. Arthritis and Rheumatism; 60:578-83.

York MR, Nagai T, Mangini AJ, Lemaire R, van Seventer JM, Lafyatis R.  2007.  A Macrophage marker, Siglec-1, is increased on circulating monocytes in patients with systemic sclerosis and induced by type-I interferons and toll-like receptor agonists. Arthritis and Rheumatism; 56:1010-20.

Lafyatis R, York M, Marshak-Rothstein A.  2006.  Antimalarial agents: Closing the gate on Toll-like receptors? Arthritis and Rheumatism; 54;3068-70.