Dr. Crow is Physician-in-Chief Emeritus at Hospital for Special Surgery, Professor of Medicine in the Division of Rheumatology of the Department of Medicine at Weill Cornell Medical College and Attending Physician at New York Presbyterian Hospital and HSS. She is also Director of the Autoimmunity and Inflammation Research Program and Co-Director of the Mary Kirkland Center for Lupus Research at the HSS Research Institute. Dr. Crow holds the Benjamin M. Rosen Chair in Immunology and Inflammation Research at HSS. She led the HSS Department of Medicine and the Division of Rheumatology in the Department of Medicine at Weill Cornell from 2010 to 2020.
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 a key pathogenic mediator in lupus. Her laboratory continues to study the triggers of immune system activation in SLE, the molecular pathways associated with the clinical manifestations of lupus and the mechanisms that result in disease flares. Dr. Crow’s research has identified therapeutic targets, providing the rationale for development of novel therapeutic agents for patients with SLE.
In addition to her leadership roles at HSS and WCMC/NYPH, Dr. Crow has served as President of the American College of Rheumatology, as President of the Henry Kunkel Society, and as Chair or Co-Chair of the Scientific Advisory Board of the Alliance for Lupus Research and the Lupus Research Alliance from 2008 to 2019. 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. In 2018 she received the Presidential Gold Medal of the American College of Rheumatology, and in 2019 she was honored as a Notable Woman in Healthcare by Crain’s New York Business.
Physician-in-Chief Emeritus, Hospital for Special Surgery
Attending Physician, Hospital for Special Surgery and NewYork-Presbyterian Hospital
Professor of Medicine, Weill Cornell Medical College
Senior Scientist, Hospital for Special Surgery Research Institute
Systemic lupus erythematosus
Arthritis Hero, Arthritis Foundation, 2001
Benjamin M. Rosen Chair in Immunology and Inflammation Research, 2002-present
Joseph P. Routh Professor of Rheumatic Diseases in Medicine, 2010-2020
Margaret D. Smith Lifetime Achievement Award, Arthritis Foundation, New York Chapter, 2010
Master, American College of Rheumatology, 2012
Honorary Member, European League Against Rheumatism, 2017
Presidential Gold Medal, American College of Rheumatology, 2018
Honoree, Notable Women in Healthcare, Crain’s New York Business, 2019
American College of Rheumatology
New York Medical and Surgical Society
American Clinical and Climatological Association
National Society for Clinical Rheumatology
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 15, 2020.
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, 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.
Kariuki SN, Crow MK, Niewold TB. The PTPN22 C1858T polymorphism is associated with skewing of cytokine profiles toward high IFN-alpha activity and low tumor necrosis factor-alpha levels in patients with lupus. Arthritis Rheum 2008; 58:2818-23.
Crow MK. Long Interspersed Nuclear Elements (LINE-1): potential triggers of systemic autoimmune disease. Autoimmunity, 2010; 43:7-16.
Crow MK. Type I interferon in the pathogenesis of lupus. J Immunol. 2014;192:5459-5468.
Mavragani CP, Sagalovskiy I, Guo Q, Nezos A, Kapsogeorgou EK, Lu P, Zhou JL, Kirou KA, Seshan SV, Moutsopoulos HM, Crow MK. Long interspersed nuclear element-1 retroelements are expressed in patients with systemic autoimmune disease and induce type I interferon. Arthritis Rheumatol. 2016; 68: 2686-2696.
Mavragani CP, Nezos A, Sagalovskiy I, Seshan S, Kirou KA, Crow MK. Defective regulation of L1 endogenous retroelements in primary Sjogren's syndrome and systemic lupus erythematosus: Role of methylating enzymes. J Autoimmun. 2018; 88:75-82.
Crow MK, Olferiev M, Kirou KA. Type I interferons in autoimmune disease. Ann Rev Pathology, 2019; 14:369-393.
Crow MK. Mitochondrial DNA promotes autoimmunity. Science, 2019, 366:1445-1446.
Navarro-Millán I, Sattui SE, Lakhanpal A, Zisa D, Siegel CH, Crow MK. Use of Anakinra to Prevent Mechanical Ventilation in Severe COVID-19: A Case Series. Arthritis Rheumatol. 2020 Jun 30:10.1002/art.41422
For more publications, please see the PubMed listing.
Dr. Crow’s research program is dedicated to elucidating the underlying mechanisms that account for initiation and amplification of immune system activation and tissue damage in systemic autoimmune diseases, with a focus on the prototype systemic autoimmune diseases, systemic lupus erythematosus (SLE) and rheumatoid arthritis. Inspired by her experience in the laboratory of Henry Kunkel, throughout her career Dr. Crow has prioritized investigation of patients, relating immunologic features of their disease to clinical manifestations, with the goal of gaining insight into disease mechanisms, identifying therapeutic targets and improving lives by stimulating development of novel therapies. Major accomplishments include identification of the type I interferon pathway as central to the pathogenesis of SLE; suggesting and supporting the hypothesis that endogenous nucleic acids, particularly those derived from genomic retroelements, might represent drivers of innate immune system activation in autoimmune disease; and relating activation of molecular pathways to clinical manifestations of disease.
Type I interferon in systemic autoimmune diseases. In the early 2000’s, Dr. Crow’s laboratory studied peripheral blood of lupus patients and healthy donors and suggested that the pattern of differential gene expression was consistent with a type I interferon signature. Subsequent studies formed the basis for the current view that the type I interferon pathway represents a major pathogenic immune mechanism in SLE and related systemic autoimmune diseases. Type I interferon-induced genes were coordinately expressed and were associated with more severe disease, and a striking association of interferon pathway activation with presence of autoantibodies specific for RNA-binding proteins was identified. Those observations formed the basis of studies that implicated Toll-like receptor 7 and recognition of RNA-containing immune complexes in type I interferon production. The laboratory developed a reporter cell assay that permitted assessment of the functional activity of the full spectrum of type I interferons in patients’ sera or plasma. This assay has been widely used to demonstrate clinical and genetic associations with type I interferon activity. Together, these studies of the type I interferon pathway, which are continuing, have re-focused understanding of lupus pathogenesis toward a significant role for the innate immune response, contributed to demonstrating a new role for autoantibodies in disease pathogenesis, identified novel endogenous triggers, identified new therapeutic targets and have provided the rationale for drug development programs targeting type I interferon, the cells that produce it, its receptor, and its downstream signaling pathway. A monoclonal antibody targeting IFNAR, the type I interferon receptor, is currently a candidate for approval by the FDA.
Genomic retroelements as candidate drivers of innate immune activation in systemic autoimmune disease. Recognizing the complexity of the human genome and the abundant representation of viral-like elements, including those that can be transcribed, translated into protein and potentially retrotranspose to a new genomic site, Dr. Crow considered the possibility that nucleic acid derived from Long Interspersed Nuclear Element-1 (LINE-1) might serve as an endogenous driver of type I interferon. Mechanisms by which LINE-1 might be involved in the altered immune function of patients with SLE were proposed. In 2016, in a study that required generation of novel reagents over a number of years, Dr. Crow’s laboratory documented increased expression of LINE-1 mRNA and its ORF1 p40 protein in epithelial cells of salivary gland tissue of patients with Sjogren’s syndrome and in renal tubular cells of patients with lupus nephritis. Importantly, induction of type I interferon by LINE-1 RNA and its inhibition with a TBK1 inhibitor suggested that cytosolic LINE-1 RNA might serve as an endogenous driver of type I interferon production. Decreased methylation of CpGs in regulatory regions of genomic LINE-1 elements in patients with SLE was shown and may contribute to the observed increased expression of LINE-1 RNA. The lab is currently collaborating with an industry partner to investigate the role of LINE-1 in activation of nucleic acid-sensing cytosolic pathways in patients with SLE.
Markers and mechanisms of lupus nephritis. Dr. Crow’s laboratory has investigated the peripheral blood transcriptome in patients with lupus nephritis and compared data from those patients to transcripts expressed in SLE patients who do not have nephritis. Through study of longitudinal blood samples from patients and analysis of gene expression in relation to clinical manifestations of disease, candidate biomarkers of lupus nephritis have been identified as well as transcripts associated with flare of nephritis. The laboratory is investigating the mechanisms through which the identified gene products contribute to renal pathology in patients with lupus nephritis.
Systemic lupus erythematosus
Type I interferon