Robert Lafyatis MD
Professor of Medicine
MD – University of Cincinnati
General field of research:
Systemic Sclerosis, Scleroderma, Fibrosis and Autoimmunity
Affiliations other than medicine:
Evans Center for Interdisciplinary Biomedical Research
Department of Molecular Medicine
Immunology Training Program
Boston University School of Medicine, E5, 72 E Concord St, Boston MA 02118
Phone: (617) 638-4312
Fax: (617) 638-5226
Research group information
Alessandra Farina, MD, PhD – Instructor
Romy de Souza, MD, PhD – Postdoctoral fellow
Allison Mathes, BS – Graduate Student
Anila Hussaini, BSRN – Clinical Coordinator
Cristina Padilla, BS – Clinical Coordinator
Michael Dimarzio – Laboratory Technician
systemic sclerosis; scleroderma; autoimmunity fibrosis
Summary of research interest:
Our laboratory effort is focused on understanding scleroderma, also known as systemic sclerosis, and developing new therapeutic approaches based on identifying biomarkers of the disease process and utilizing biomarkers in clinical trials. Our group has a particular interest in understanding the mechanisms stimulating the immune response in the disease, focusing on innate immune responses leading to fibrosis and vascular injury. Our data show increased expression of interferon responsive genes in circulating monocytes of scleroderma patients, prompting current investigations into the stimulus for this pattern of gene expression and the effect of interferon on fibrosis and vascular injury. We are also investigating the pathogenesis through existing models of scleroderma, testing novel therapeutics in thee models and developing new murine models designed to clarify the relationship between innate immunity and fibrosis.
Aliprantis, A.O., J. Wang, J.W. Fathman, R. Lemaire, D.M. Dorfman, R. Lafyatis, L.H. Glimcher. 2007. Transcription factor T-bet regulates skin sclerosis through its function in innate immunity and via IL-13. Proc Natl Acad Sci U S A 104(8): 2827-30.
Bayle, J., J. Fitch, K. Jacobsen, R. Kumar, R. Lafyatis, R. Lemaire. 2008. Increased expression of Wnt2 and SFRP4 in Tsk mouse skin: role of Wnt signaling in altered dermal fibrillin deposition and systemic sclerosis. J Invest Dermatol 128(4): 871-81.
Farina, G., R. Lemaire, P. Pancari, J. Bayle, R.L. Widom, R. Lafyatis. 2009. Cartilage oligomeric matrix protein expression in systemic sclerosis reveals heterogeneity of dermal fibroblast responses to transforming growth factor beta. Ann Rheum Dis 68(3): 435-41.
Kissin, E.Y., P.A. Merkel, R. Lafyatis. 2006. Myofibroblasts and hyalinized collagen as markers of skin disease in systemic sclerosis. Arthritis Rheum 54(11): 3655-60.
Lafyatis, R., E. Kissin, M. York, G. Farina, K. Viger, M.J. Fritzler, P.A. Merkel, R.W. Simms. 2009. B cell depletion with rituximab in patients with diffuse cutaneous systemic sclerosis. Arthritis Rheum 60(2): 578-83.
Richez, C., K. Yasuda, A.A. Watkins, S. Akira, R. Lafyatis, J.M. van Seventer, I.R. Rifkin. 2009. TLR4 ligands induce IFN-alpha production by mouse conventional dendritic cells and human monocytes after IFN-beta priming. J Immunol 182(2): 820-8.
York M.R., T. Nagai, A.J. Mangini, R. Lemaire, J.M. van Seventer, R. Lafyatis. 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 Rheum 56(3): 1010-20.
Technologies available for sharing upon request:
primary dermal fibroblast culture; real-time PCR analysis of skin gene expression; animal models of scleroderma