Mary K. Crow, M.D., is Physician-in-Chief Emeritus at Hospital for Special Surgery, Professor of Medicine at Weill Cornell Medical College, and Professor of Immunology in its Graduate School of Medical Sciences. Dr. Crow is also Senior Scientist, Co-Director of the Mary Kirkland Center for Lupus Research, and Director of the Autoimmunity and Inflammation Program at Hospital for Special Surgery's Research Institute where she holds the Benjamin M. Rosen Chair in Immunology and Inflammation Research. Dr. Crow received her M.D. from Cornell University Medical College, Internal Medicine and Rheumatology subspecialty training at New York Hospital and Hospital for Special Surgery, and post-doctoral research training at Rockefeller University. The overall goal of Dr. Crow's research program is to elucidate the underlying mechanisms that account for initiation and amplification of altered immune function and tissue damage in systemic autoimmune diseases, with a particular focus on the prototype systemic autoimmune diseases, systemic lupus erythematosus (SLE) and rheumatoid arthritis. Dr. Crow identified the type I interferon (IFN) pathway as central to the pathogenesis of SLE, and she continues to investigate the cellular and cytokine mediators of immune system activation and inflammation in those disorders. Current interests include the role of endogenous RNA, including genomic retroelements, in IFN pathway activation in systemic autoimmune diseases, along with the role of Toll-like receptor (TLR)-dependent and TLR-independent pathways in innate immune system activation in those disorders. She is also investigating the immune mechanisms that are associated with development of lupus nephritis.
Dr. Crow's leadership roles have included president of the American College of Rheumatology, president of the Henry Kunkel Society, and chair of the Scientific Advisory Board of the Lupus Research Alliance. In 2017 Dr. Crow was named an honorary member of the European League Against Rheumatism, in 2018 she received the Presidential Gold Medal of the American College of Rheumatology in recognition of outstanding contributions to rheumatology over an entire career, and in 2022 she received the Lee C. Howley Sr. Prize for Arthritis Scientific Research from the Arthritis Foundation.
Mary Kirkland Center for Lupus Research
Systemic lupus erythematosus
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Physician-in-Chief Emerita, Hospital for Special Surgery
Attending Physician, Hospital for Special Surgery and NewYork-Presbyterian Hospital
Professor of Medicine, Weill Cornell Medical College and Weill Graduate School of Medical Sciences
Senior Scientist, Hospital for Special Surgery Research Institute
Lee C. Howley Sr. Prize for Arthritis Scientific Research, Arthritis Foundation, 2022
Benjamin M. Rosen Chair in Immunology and Inflammation Research, 2002-present
Joseph P. Routh Professor of Rheumatic Diseases in Medicine, 2010-2020
Honoree, Notable Women in Healthcare, Crain’s New York Business, 2019
Presidential Gold Medal, American College of Rheumatology, 2018
Honorary Member, European League Against Rheumatism, 2017
Master, American College of Rheumatology, 2012
Margaret D. Smith Lifetime Achievement Award, Arthritis Foundation, New York Chapter, 2010
Arthritis Hero, Arthritis Foundation, 2001
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
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
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Below are the healthcare industry relationships reported by Dr. Crow as of August 18, 2023.
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