Jane E Salmon   Associate Dean of Faculty Affairs

Phone
  • +1 212 606 1422

Dr. Jane Salmon is the Collette Kean Research Professor at Hospital for Special Surgery. She is Professor of Medicine and Professor of Medicine in Obstetrics and Gynecology and Associate Dean, Faculty Affairs at Weill Cornell College of Medicine.

Dr. Salmon graduated magna cum laude from New York University and earned a medical degree in 1978 from the College of Physicians and Surgeons of Columbia University, where she was the first woman enrolled in their Medical Scientist Training Program. She completed training in internal medicine at The New York Hospital and in rheumatology at Hospital for Special Surgery, where she currently conducts clinical and basic research studies and practices rheumatology. Dr. Salmon has served on the Board of Directors of the American College of Rheumatology and Rheumatology Research Foundation. Dr. Salmon was co-editor of Arthritis and Rheumatism and is currently an Associate Editor of Annals of Rheumatic Diseases. At Hospital for Special Surgery, she is a Director of the Lupus and APS Center of Excellence, co-Director of the Mary Kirkland Center for Lupus Research.

Dr. Salmon’s research has focused on elucidating mechanisms of tissue injury in lupus and other autoimmune diseases. Her basic, translational and clinical studies have led to a paradigm shift in the understanding of mechanisms of pregnancy loss, cardiovascular disease and end-organ damage in patients with lupus. She identified the critical role of inflammation as a mediator of placental insufficiency and defined new treatment targets.

Appointments
Attending Physician, Hospital for Special Surgery Collette Kean Research Chair, Hospital for Special Surgery
Director, SLE APS Center of Excellence, Hospital for Special Surgery
Senior Scientist, Hospital for Special Surgery
Co-Director, Mary Kirkland Center for Lupus Research, Hospital for Special Surgery
Professor of Medicine, Weill Cornell Medical College 
Professor of Medicine in Obstetrics and Gynecology, Weill Cornell Medical College 
Professor, Graduate Program in Microbiology and Immunology, Weill Cornell Graduate School of Medical Sciences
Associate Dean of Faculty Affairs, Weill Cornell Medicine

Specialty
Rheumatology
Internal Medicine

Special Expertise
Systemic Lupus 
Erythematosus Antiphospholipid Syndrome
Rheumatoid Arthritis

Awards
Elected member, National Academy of Medicine, 2016 
Master, American College of Rheumatology, 2017 
Evelyn Hess Award, Lupus Foundation of America, 2014 
Swartz Lectureship, Swedish Society of Medicine, 2012 
Virginia Kneeland Frantz ’22 Distinguished Women in Medicine Award, Columbia P&S Alumni Association, 2012 
New York Magazine: Top Doctors: 2013, 2012, 2009, 2004 
American Association of Physicians 2008 Carol Nachman Prize in Rheumatology (most prestigious international award for rheumatology), 2007 
Theodore E. Woodward Award, American Clinical and Climatological Association, 2007

Publications

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Selected publications

Research

research overview

  • Dr. Salmon’s research goal is to identify predictors and determinants of disease phenotype in systemic lupus erythematosus (SLE) and related diseases, and to thereby identify targets for therapy. In SLE and other autoimmune diseases, autoantibodies and immune complexes initiate inflammation and organ damage through receptors for IgG and complement activation products. The laboratory investigates downstream mediators and effector mechanisms of tissue injury. Their basic, translational and clinical studies have led to a paradigm shift in the understanding of mechanisms of pregnancy loss, cardiovascular disease and nephritis in patients with SLE. This work to define pathogenic mechanisms in SLE is likely to translate to non-autoimmune patients.

    Dr. Salmon’s laboratory defined structure-function relationships among human receptors for IgG, key effectors in immune-complex diseases and showed that allelic variants were risk factors for nephritis. She led the first case-control study to define prevalence and clinical correlates of pre-clinical atherosclerosis in SLE and found accelerated and premature disease, independent of traditional cardiovascular risk factors, rather related to inflammation.

    Building on her discovery that innate immune pathways, complement, neutrophils and TNF-α, are critical effectors of pregnancy complications in mouse models, she led an NIH-funded, multi-center 11 year prospective longitudinal study of 700 pregnant patients to identify predictors of pregnancy outcomes in patients with lupus and/or anti-phospholipid syndrome. She has now embarked on the first interventional trial of biologic therapy to protect pregnancies at high risk for preeclampsia, an approach likely to have broad public health implications.

    Pregnancy Loss and Preeclampsia in Patients with Systemic Lupus Erythematosus and Antiphospholipid Antibodies
    The antiphospholipid syndrome (APS) is characterized by thrombosis and pregnancy loss that occur in the presence of antiphospholipid (aPL) antibodies. APS is a leading cause of pregnancy loss and pregnancy-related morbidity. The pathogenesis of fetal loss and growth restriction in APS is incompletely understood, and treatment is suboptimal. Currently, therapy for pregnant women with APS is focused on preventing thrombosis, but anticoagulation is only partially successful in averting miscarriage and carries risks for fetus and mother. The Salmon laboratory identified the critical role of inflammation as a mediator of placental insufficiency, in general, and defined new treatment targets.

    We proposed that complement activation is a central mechanism of pregnancy loss in APS, and demonstrated that this novel hypothesis was valid in an experimental animal model of aPL antibody-induced fetal death. We found that inhibition of the complement cascade in vivo blocks fetal loss and growth restriction associated aPL antibodies and, using genetically manipulated mice, blocking antibodies and small molecules, identified specific complement components and the downstream mediator, TNF-alpha, as key effectors of placental damage. We are using similar approaches to characterize mediators of preeclampsia in antibody-independent experimental models. Identification of the drivers of placental insufficiency will provide the basis for new therapies to improve outcomes in pregnant women with SLE, APS and, potentially, in pregnancy loss and preeclampsia in non-autoimmune patients.

    To translate to patients the discovery in mouse models that innate immune pathways, complement, neutrophils and TNF-α, are critical effectors of pregnancy complications, Dr. Salmon led the PROMISSE (Predictors of pRegnancy Outcome: bioMarkers In antiphospholipid antibody Syndrome and Systemic lupus Erythematosus) Study, an NIH-funded, multi-center 11 year prospective longitudinal study of pregnant patients. The goal of PROMISSE was to identify predictors of pregnancy outcomes in patients with lupus and/or aPL. We have recruited over 700 pregnant patients, enrolled at nine major clinical centers, and obtain detailed medical and obstetrical information during the course of their pregnancies, and serial blood specimens for biomarkers. Demographic, socioeconomic and potential circulating inflammatory mediators, complement activation products and biomarkers of placental dysfunction are analyzed every month of pregnancy to establish a pregnancy risk profile, and we continue to mine the data and sample collection. In addition, we are analyzing RNA obtained through pregnancy to compare temporal changes in gene expression during the course of complicated and uncomplicated pregnancies and to understand immune regulation in pregnancy and identify predictors of poor outcomes. The identification of markers in aPL and SLE patients may prove generally applicable to anticipate complications during pregnancy in disease-free women.

    Characterization of clinically applicable surrogate markers that predict severe pregnancy complications have enabled us to design an interventional trial. And now, we have embarked on the first interventional trial of biologic therapy to protect pregnancies at high risk for preeclampsia, an approach likely to have broad public health implications.

    Accelerated Cardiovascular Disease in Systemic Lupus Erythematosus and Rheumatoid Arthritis: Prevalence and Responsible Mechanisms
    Autopsy and observational data suggest that SLE is associated with premature atherosclerosis and myocardial infarction. The prevailing hypothesis has been that accelerated atherosclerosis is attributable to an increased frequency of conventional risk factors in SLE patients, such as hypertension and hyperlipidemia, which may be provoked or potentiated by therapeutic use of corticosteroids. However, data are accumulating that suggest that the inflammatory process per se may be important in the initiation and progression of atherosclerosis.

    We performed the first case-control study to assess the presence, magnitude, and determinants of atherosclerosis in SLE and its correlates in a population-based sample of 200 SLE patients and 200 matched disease-free controls. Although SLE patients and controls were comparable in traditional cardiovascular disease risk factors, atherosclerosis, detected by carotid ultrasound, was more prevalent in SLE patients (37 vs. 15%, p<0.001). The excess in atherosclerosis was most pronounced in the youngest patients (5.6-fold increase in SLE patients less than 40 years of age). We identified the presence of SLE as the most important independent correlate of atherosclerosis other than age. Clinical features and autoantibody specificities differentiated SLE patients with and without plaque. Our case control study of patients with rheumatoid arthritis revealed increased and accelerated atherosclerosis, comparable to that of SLE. This work supports the possibility that chronic inflammation per se predisposes to premature cardiovascular disease and suggests that therapies directed at inflammation might prevent atherosclerosis. Ongoing work examining endothelial cell gene expression and assessing levels of potential biomarkers in the circulation will test this hypothesis and elucidate mechanisms of accelerated atherosclerosis in patients with SLE and other autoimmune diseases.

    Mediators and Mechanisms of End-Organ Damage in SLE and Related Diseases
    Immune complex deposition activates neutrophils, increases vascular permeability and leads to organ damage in SLE and RA. Dr. Salmon’s laboratory has been exploring novel approaches to attenuate tissue injury initiated by immune complexes and downstream mediators they drive. The bioactive lipid sphingosine-1-phosphate (S1P), acting via S1P receptor 1 (S1P1), is a key regulator of endothelial cell barrier function. We found that S1P1 signaling in endothelial cells prevents loss of barrier integrity induced by activated neutrophils and attenuates animal models of acute inflammatory injury mediated by immune complexes. Current studies will determine whether the S1P-S1P receptor axis can be targeted to prevent organ damage in experimental models of SLE and rheumatoid arthritis. In parallel, we will assess S1P-S1P receptor expression in tissue from patients.

    Lupus nephritis often results in progressive renal dysfunction. The inactive Rhomboid 2 (iRhom2) is a newly identified key regulator of A disintegrin and metalloprotease 17 (ADAM17), whose substrates, such as TNF- and heparin-binding epidermal growth factor (HB-EGF), have been implicated in the pathogenesis of chronic kidney disease. We demonstrate that deficiency of iRhom2 protects the lupus-prone mice from developing severe kidney damage without altering autoantibody production, by simultaneously blocking the HB-EGF/EGFR and the TNF- signaling in the kidney tissues. Kidneys from lupus nephritis patients showed increased iRhom2 and HB-EGF expression which associates with severe irreversible damage. Studies are ongoing to explore this novel target for selective and simultaneous dual inhibition of two major pathological pathways in the effector arm of lupus nephritis.

Background

Contact

Primary Email

  • jes2002@med.cornell.edu