Mary K. Crow, MD

Dr. Crow is Associate Chief, Division of Rheumatology and Director of Rheumatology Research at Hospital for Special Surgery. She combines basic and translational research on the mechanisms that underlie systemic autoimmune diseases with active participation in the clinical and academic programs of the hospital and Weill Medical College of Cornell University. Patients with systemic lupus erythematosus, rheumatoid arthritis and scleroderma have made important contributions to the understanding of those diseases through their participation in Dr. Crow’s research. Dr. Crow serves as Co-Director of the Mary Kirkland Center for Lupus Research and Director of the Autoimmunity and Inflammation Research Program at Hospital for Special Surgery.

 

Appointments

Attending Physician, Hospital for Special Surgery

Attending Physician, New York Presbyterian Hospital

Professor of Medicine, Weill Medical College of Cornell University

Senior Scientist, Hospital for Special Surgery

Specialty

Rheumatology Division

Internal Medicine

Special Expertise

Systemic lupus erythematosus

Rheumatoid arthritis

Awards

Arthritis Hero, Arthritis Foundation, 2001

Benjamin M. Rosen Chair in Autoimmunity and Inflammation Research, 2002

Affiliations

American College of Rheumatology, President-Elect

Member, Medical Advisory Committee, The S.L.E. Foundation, Inc.

Specialized Centers

Mary Kirkland Center for Lupus Research

Education

MD, 1978, Cornell University Medical College, New York

Internship

New York Hospital, Internal Medicine, New York, 1978-1979

Residency

New York Hospital, Internal Medicine, New York, 1979-1981

Fellowship

Rockefeller University, Immunology Research, New York, 1981-1984

Hospital for Special Surgery, Rheumatology, New York, 1981-1984

Certification

Internal Medicine, Rheumatology

State Licensure

New York  

Mary K. Crow, MD is the author of the following articles on HSS.edu:

For Patients

For Professionals

 

Selected Publications

Chernysheva AD, Kirou KA, Crow MK. T cell proliferation induced by autologous non-T cells is a response to apoptotic cells processed by dendritic cells. J Immunol 169:1241-1250, 2002.

Roman MJ, Shanker B-A, Davis A, Lockshin MD, Sammaritano L, Simantov R, Crow MK, Schwartz JE, Paget SA, Devereux RB, Salmon JE. Prevalence and correlates of accelerated atherosclerosis in systemic lupus erythematosus. N Engl J Med 349:2399-406, 2003.

Crow MK, Kirou KA, Wohlgemuth J. Microarray analysis of interferon-regulated genes in SLE. Autoimmunity 36:481-490, 2003.

Crow MK. Type I interferon and autoimmune disease. Autoimmunity 36:445-446, 2003.

Crow MK: Costimulatory molecules and T cell-B cell interactions. Rheum Dis Clin N Amer, 30:175-191, 2003.

Crow MK, Kirou KA. Interferon-alpha in systemic lupus erythematosus. Curr Opin Rheum, 16:541-547, 2004.

Liu S, Cerutti A, Casali P, Crow MK. Ongoing immunoglobulin class switch DNA recombination in lupus B cells: analysis of switch regulatory sequences. Autoimmunity, 37:431-443, 2004.

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, 50:3958-67, 2004.

Kirou KA, Lee C, George S, Louca K, Peterson MGE, Crow MK. Interferon-alpha pathway activation identifies a subgroup of systemic lupus erythematosus patients with distinct serologic features and active disease. Arthritis Rheum, 52:1491-503, 2005.

Roman MJ, Devereux RB, Schwartz JE, Lockshin MD, Paget SA, Davis A, Crow MK, Sammaritano L, Levine DM, Shankar B-A, Moeller E, Salmon JE. Arterial Stiffness in Chronic Inflammatory Diseases. Hypertension, 46:194-9, 2005.

For more publications, please see the PubMed listing.  

Research Description

Immunoregulation in Autoimmune and Inflammatory Diseases

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. In systemic lupus erythematosus (SLE), the prototype systemic autoimmune disease, proteins present in intracellular particles, along with the DNA or RNA bound by those proteins, are targeted by lymphocytes and antibodies of the immune system, resulting in inflammation and widespread tissue damage. This autoreactive immune response is mediated by CD4+ helper T lymphocytes that orchestrate a coordinated program of immune and inflammatory functions through interactions with B lymphocytes, macrophages, dendritic cells, as well as cells outside the immune system, such as the endothelial cells that line blood vessels. The goals of the laboratory are to define the triggers of immune activation in autoimmune disease and to characterize the mechanisms used by the immune system to regulate the effector cells that contribute to inflammation and tissue damage.

A current paradigm proposes that apoptotic cells may serve as a source of the self-antigens that initiate autoimmunity. However, all individuals are exposed to apoptotic cells. Our challenge is to understand why some individuals develop autoimmune disease and others do not. We propose that while apoptotic cells may serve as one source of self-antigen, adjuvant-like factors in the immune microenvironment of some individuals promote the effective presentation of available antigens to CD4+ T cells, resulting in T cell activation and generation of effector mechanisms targeted at self-antigens. Active projects include identification of the stimuli and molecular pathways involved in induction of type I interferon in SLE, with genome-derived immunostimulatory DNA and double stranded or single stranded RNA potential mediators of this effect; characterization of proinflammatory gene products produced in SLE and associated with active disease; and investigation of the relationship between interferon pathway activation and production of specific autoantibodies, particularly those targeting RNA-binding proteins.

As clinical investigators, we search for applications of our laboratory studies that may have impact on patients with disease. Efforts underway are aimed at identifying novel approaches to inhibition of the type I interferon pathway that may inform development of new therapeutic interventions in SLE. We are identifying the gene products that are differentially expressed between SLE patients with and without accelerated atherosclerosis, with the aim of characterizing novel targets that could modulate development of this clinically important outcome. Finally, we are studying the contribution of immune system activation and inflammation to disease in patients with osteoarthritis.

Research Interests

Mechanisms of autoimmune disease, Genomic triggers of autoimmunity, Systemic lupus erythematosus, Rheumatoid arthritis, Scleroderma

Clinical Trials