Dr. Crow is Physician-in-Chief and Chair of the Department of Medicine at Hospital for Special Surgery and is Chief of the Division of Rheumatology at HSS and NewYork-Presbyterian/Weill Cornell Medical Center. She is also Director of the Autoimmunity and Inflammation Research Program and Co-Director of the Mary Kirkland Center for Lupus Research at HSS. Dr. Crow holds the Benjamin M. Rosen Chair in Immunology and Inflammation Research at HSS and is the Joseph P. Routh Professor of Rheumatic Diseases in Medicine at Weill Cornell Medical College.
Dr. Crow leads 66 full-time physicians, including 30 adult and 3 pediatric rheumatologists, who provide outstanding care to patients across the full spectrum of autoimmune and inflammatory rheumatic diseases and deliver perioperative medical care to patients undergoing surgical procedures at HSS. Dr. Crow has established disease-specific Centers of Excellence focused on innovative initiatives in clinical and translational research, patient and professional education, and quality of care.
Dr. Crow’s academic and research career has focused on unraveling the cellular and molecular mechanisms that underlie the systemic autoimmune diseases, with a particular focus on systemic lupus erythematosus and rheumatoid arthritis. She has identified interferon-alpha, an immune system protein typically expressed in the setting of virus infection, as the key pathogenic mediator in lupus. Her laboratory continues to study the molecular pathways that are associated with the clinical manifestations of lupus and the mechanisms that result in disease flares.
In addition to her leadership roles at HSS and NYPH/WCMC, Dr. Crow has served as President of the American College of Rheumatology and as President of the Henry Kunkel Society. She has been honored as an “Arthritis Hero” of the Arthritis Foundation, and in 2010 she received the Margaret D. Smith Lifetime Achievement Award of the Arthritis Foundation, New York Chapter.
Physician-in-Chief, Hospital for Special Surgery
Chair, Department of Medicine, Hospital for Special Surgery
Chief, Division of Rheumatology, Hospital for Special Surgery, New York Presbyterian Hospital and Weill Cornell Medical College
Senior Research Scientist, Hospital for Special Surgery
Professor of Medicine, Weill Cornell Medical College
Attending Physician, Hospital for Special Surgery and New York Presbyterian Hospital
Systemic lupus erythematosus
Arthritis Hero, Arthritis Foundation, 2001
Benjamin M. Rosen Chair in Immunology and Inflammation Research, 2002
Joseph P. Routh Professor of Rheumatic Diseases in Medicine, 2010
Margaret D. Smith Lifetime Achievement Award, Arthritis Foundation, New York Chapter, 2010
American College of Rheumatology, President-Elect
Member, Medical Advisory Committee, The S.L.E. Foundation, Inc.
One of the goals of HSS is to advance the science of orthopedic surgery, rheumatology, and related disciplines for the benefit of patients. Physicians at HSS may collaborate with outside companies for education, research and medical advances. HSS supports this collaboration in order to foster medical breakthroughs; however HSS also believes that these collaborations must be disclosed.
As part of the disclosure process, this website lists physician collaborations with outside companies. The disclosures are provided by information provided by the physician and other sources and are updated regularly. Further information may be available on individual company websites.
Below are the healthcare industry relationships reported by Dr. Crow as of September 19, 2019.
By disclosing the collaborations of HSS physicians with industry on this website, HSS and its physicians make this information available to their patients and the public, thus creating a transparent environment for those who are interested in this information. Further, the HSS Conflicts of Interest Policy does not permit physicians to collect royalties on products developed by him/her that are used on patients at HSS.
Patients should feel free to ask their HSS physicians questions about these relationships.
MD, Weill Cornell Medical College, New York, 1978
New York Hospital, Internal Medicine, New York, 1978-1979
New York Hospital, Internal Medicine, New York, 1979-1981
Post-doctoral Research Fellowship: Rockefeller University, Immunology Research, New York, 1981-1984
Clinical Fellowship: Hospital for Special Surgery, Rheumatology, New York, 1981-1984
Crow MK. Interferon-alpha: A new target for therapy in systemic lupus erythematosus? Arthritis Rheum 2003; 48:2396-401.
Crow MK, Wohlgemuth J. Microarray analysis of gene expression in lupus. Arthritis Res Ther 2003; 5:279-87.
Crow MK, Kirou KA, Wohlgemuth J. Microarray analysis of interferon-regulated genes in SLE. Autoimmunity 2003; 36:481-90.
Kirou KA, Lee C, George S, Louca K, Papagiannis IG, Peterson MGE, Ly N, Woodward RN, Fry KE, Lau A Y-H, Prentice JG, Wohlgemuth JG, Crow MK. Coordinate overexpression of interferon-alpha-induced genes in systemic lupus erythematosus. Arthritis Rheum 2004; 50:3958-67.
Kirou KA, Lee C, George S, Louca K, Peterson, Crow MK. Interferon-alpha pathway activation identifies a subgroup of systemic lupus erythematosus patients with distinct serologic features and active disease. Arthritis Rheum 2005; 52:1491-503.
Hua J, Kirou K, Lee C, Crow MK. Functional assay of type I interferon in systemic lupus erythematosus plasma and association with anti-RNA binding protein autoantibodies. Arthritis Rheum 2006; 54:1906-16.
Niewold TB, Hua J, Lehman TJA, Harley JB, Crow MK. High serum interferon alpha activity is a heritable risk factor for systemic lupus erythematosus. Genes Immun 2007; 8:492-502.
Niewold TB, Kelly JA, Flesch MH, Espinoza LR, Harley JB, Crow MK. Association of the IRF5 risk haplotype with high serum interferon-alpha activity in systemic lupus erythematosus patients. Arthritis Rheum 2008; 58:2481-7.
Crow MK. Collaboration, genetic associations, and lupus erythematosus. New Engl J Med 2008; 358:956-61.
Mavragani CP, La DT, Stohl W, Crow MK. Association of the response to TNF antagonists with plasma type I interferon activity and interferon-beta/alpha ratios in rheumatoid arthritis patients: a post-hoc analysis of a predominantly Hispanic Cohort. Arthritis Rheum, 2010; 62:392-401.
Crow MK. Developments in the clinical understanding of lupus. Arthritis Res Ther, 2009; 11:245.
Crow MK. Long Interspersed Nuclear Elements (LINE-1): potential triggers of systemic autoimmune disease. Autoimmunity, 2010; 43:7-16.
Crow MK. Interferon-alpha: a therapeutic target in systemic lupus erythematosus. Rheum Dis Clin North Am, 2010; 36:173-86.
Crow MK. Interferon-alpha in systemic lupus erythematosus. In: Systemic Lupus Erythematosus. Fifth Edition. Edited by Robert G. Lahita. Elsevier 2011; 307-320.
Crow MK. Systemic Lupus Erythematosus. In: Cecil’s Textbook of Medicine. 24rd Edition. Edited by Goldman and Schafer. Elsevier 2011; 1697-1705.
For more publications, please see the PubMed listing.
The immune system has evolved to maintain the integrity of the organism in an environment rich in infectious microbes. When the immune system becomes misdirected toward components of one’s own tissue, autoimmune disease and chronic inflammation can result. The hypothesis that forms the basis of Dr. Crow’s research program is that in systemic autoimmune disease, with systemic lupus erythematosus (SLE) the prototype, endogenous nucleic acids that are similar to viral or bacterial nucleic acids induce chronic immune system activation and clinical disease that mimics a chronic and poorly controlled viral infection.
In SLE, activation of the innate immune system by viral-like nucleic acids results in production of type I interferon (IFN), with IFN-alpha the major component of the response. IFN-alpha primes the immune system to become reactive to self-proteins, and when self-reactive antibodies are formed, immune complexes containing RNA or DNA and the proteins bound by those nucleic acids can amplify immune system activation and augment production of IFN-alpha. Dr. Crow’s laboratory studies molecular pathways that involve nucleic acid receptors present in the cytoplasm as well as those mediated by endosomal Toll-like receptors. The nature of the nucleic acids that stimulate those pathways is a particular interest. It is proposed that persistent production of IFN-alpha is a feature of many lupus patients and can contribute to immune dysregulation, inflammation and widespread tissue damage. The laboratory’s studies, along with those of other investigators, provide the strong rationale for development of therapeutics that target the nucleic acid triggers, receptors and protein products that result from innate immune system activation. IFN-alpha and the Toll-like receptor pathways that amplify IFN production are rational therapeutic targets supported by Dr. Crow’s research.
Close collaboration among investigators in the laboratory and clinical rheumatologists at HSS has permitted generation of longitudinal data from lupus patients and collection of associated blood samples. Detailed clinical characterization of patient disease activity, along with analysis of gene expression and plasma proteins in relation to clinical disease flares, has allowed identification of molecular pathways that are associated with clinical manifestations of disease, disease activity and disease flares. A goal of the laboratory is to identify the molecular precursors of future disease flares, permitting timely institution of disease-modifying therapy.
Mechanisms of autoimmune disease
Genomic triggers of autoimmunity
Type I interferon
Systemic lupus erythematosus