Jane E. Salmon, MD

Dr. Jane Salmon is Professor of Medicine and Professor of Obstetrics and Gynecology at Weill Cornell Medical College and the Collette Kean Research Professor at Hospital for Special Surgery.

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, and has been an HSS faculty member since 1983. Dr. Salmon has served on the Board of Directors of the American College of Rheumatology and as Councilor of the Clinical Immunology Society. She serves on the NIH Advisory Boards for the North American Rheumatoid Arthritis Consortium, the Lupus Multiplex Registry, and the Consortium for the Longitudinal Evaluation of African-Americans with Early RA. She is currently a co-editor of Arthritis and Rheumatism. At Hospital for Special Surgery, she is a co-Director of the Mary Kirkland Center for Lupus Research, Director of the FOCIS Center of Excellence, and Director of the Lupus Registry and Repository.

Dr. Salmon’s research has focused on elucidating mechanisms of tissue injury in lupus and other autoimmune diseases. Her basic and clinical studies have expanded our understanding of pregnancy loss and organ damage in SLE and the determinants of disease outcome in lupus patients with nephritis, pregnancy, and cardiovascular disease.

Appointments

Attending Physician, Hospital for Special Surgery
Collette Kean Research Chair, Hospital for Special Surgery
Senior Scientist, Hospital for Special Surgery
Co-Director, Mary Kirkland Center for Lupus Research, Hospital for Special Surgery
Director of the Lupus Registry and Repository, Hospital for Special Surgery
Professor of Medicine, Weill Cornell Medical College
Professor of Medicine in Ostetrics and Gynecology, Weill Cornell Medical College
Professor, Graduate Program in Immunology, Weill Cornell Graduate School of Medical Sciences

Specialty

Rheumatology
Internal Medicine

Special Expertise

Systemic Lupus Erythematosus
Antiphospholipid Syndrome
Rheumatoid Arthritis

Awards

"Best Doctors in New York," New York magazine, 2009
Carol Nachman Prize in Rheumatology, 2007
Eric Bywaters Memorial Lecture, Imperial College of London, 2007
Edmund L. Dubois, MD, Memorial Lectureship Award, American College of Rheumatology, 2004
Henry Christian Award for Excellence in Research, from the American Federation for Clinical Research, 1992
Arthritis Investigator of the Arthritis Foundation, 1984

Affiliations

FOCIS Centers of Excellence Committee
Scientific Programme Committee, European League Against Rheumatism (EULAR)

Specialized Centers

• Mary Kirkland Center for Lupus Research

Education

MD, Columbia University College of Physicians and Surgeons, New York

Residency

The New York Hospital, New York, New York

Fellowship

Hospital for Special Surgery, Fellow in Rheumatic Diseases

Certification

Rheumatology
Internal Medicine

State Licensure

New York  

Jane E. Salmon, MD is the author of the following articles on HSS.edu:

Editorial Appointments

Editorial Board, Lupus
Co-Editor, Arthritis and Rheumatism

Selected Publications

Roman MJ, Crow MK, Lockshin MD, Devereux RB, Paget SA, Sammaritano, L, Levine DM, Davis A, Salmon JE. Rate and Determinants of Progression of Atherosclerosis in Systemic Lupus Erythematosus. Arthritis Rheum 56: 3412-19, 2007.

Roman MJ, Salmon JE. Cardiovascular Manifestations of Rheumatologic Diseases. Circulation 116: 2346-2355, 2007.

Girardi G, Yarilin D, Thurman JM, Holers VM, Salmon JE. Complement Activation Induces Dysregulation of Anglogenic Factors and Causes Fetal Rejection and Growth Restriction. J Exp Med 203: 2165-2175, 2006.

Roman M, Moeller E, Davis A, Paget SA, Crow MK, Lockshin MD, Sammaritano L, Devereux RB, Schwartz JE, Levine DM, Salmon JE. Preclinical Carotid Atherosclerosis in Patients with Rheumatoid Arthritis: Prevalence and Associated Factors. Ann Intern Med 144: 249-256, 2006.

Girardi G, Redecha PB, Salmon JE. Heparin Prevents Antiphospholipid Antibody-induced Fetal Loss by Inhibiting Complement Activation. Nat Med 10:1222-6, 2004.

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. New Engl J Med 349: 2399-406, 2003.

Girardi G, Berman J, Redecha P, Spruce L, Thurman JM, Kraus D, Hollmann TJ, Casali P, Caroll MC, Wetsel RA, Lambris JD, Holers VM, Salmon JE. Complement C5a Receptors and Neutrophils Mediate Fetal Injury in the Antiphophospholipid Syndrome. J Clin Invest 112: 1644-54, 2003.

Salmon JE, Pricop L: Human Receptors for Immunoglobulin G: Key Elements in the Pathogenesis of Rheumatic Disease. Arthritis Rheum 44: 739-750, 2001.

Salmon JE, Millard SS, Schachter LA, Arnett FC, Ginzler EM, Gourley MF, Ramsey-Goldman R, Kimberly RP: FcgRIIA alleles are heritable risk factors for lupus nephritis in African Americans. J Clin Invest 97: 1348-1354, 1996.

For more publications, please see the PubMed listing.

Selected Books/Chapters

Salmon JE, Kimberly RP, D’Agati V: Immunopathology of SLE. in: Rheumatology 3rd Edition, edited by MC Hochberg, AJ Silman, JS Smolen, ME Weinblatt, M Weisman. Mosby, London, pp 1297-1322, 2003; 4th edition, in press 2005.

Salmon JE. Mechanisms of Immune-mediated Injury. in: Cecil Textbook of Medicine (22nd edition), edited by L Goldman and D Ausiello, Saunders, Philadelphia, pp 223-227, 2004.

Salmon JE. Girardi G: The role of complement in the antiphospholipid syndrome. in: Current Directions in Autoimmunity, edited by G Tsokos. Karger, Basel, vol 7, pp 133-148, 2004.

Manzi S, Ahearn JM, Salmon JE. New Insights into Complement: A Mediator of Injury and Marker of Disease Activity in SLE. Lupus 13: 298-303, 2004.

Girardi G, Salmon JE. The Role of Complement in Antiphospholipid Antibody-Induced Pregnancy Loss and Thrombosis. in: Hughes Syndrome: Antiphospholipid Syndrome, 2nd edition, edited by M Khamashta, Springer-Verlag Ltd, London, in press.

Selected Presentations

Eric Bywaters Memorial Lectureship, Imperial College of London, UK, 2007
Arthur DeGraff Lecture, New York University School of Medicine, 2007
Dr. Jacob Probstein Endowed Lecture in Obstetrics and Gynecology, Washington University in St. Louis, 2004
Janice M. Wiles Memorial Lecture on SLE, University of Massachusetts, 2001
Kroc Visiting Professor, UCLA, 1997  

Research Description

Inflammatory Effector Mechanisms Laboratory

The goal of our research is to identify determinants of disease phenotype in systemic lupus erythematosus (SLE) and related diseases, and to thereby identify targets for therapy. Our laboratory approach is to study effector function and mechanisms of tissue injury. In SLE and other autoimmune diseases, autoantibodies and immune complexes trigger inflammation and organ damage through receptors for Ig (FcgR) and complement activation products. These mechanisms are currently studied in three projects.

The Role of Complement Activation in Antiphospholipid Antibody-induced Pregnancy Loss and Thrombosis

The antiphospholipid syndrome (APS) is characterized by thrombosis and pregnancy loss that occur in the presence of antiphospholipid (aPL) antibodies. Over the last two decades, APS has emerged as 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. We recently proposed that complement activation is a central mechanism of pregnancy loss in APS, and demonstrated that this novel hypothesis was valid in a mouse model of aPL antibody-induced fetal death. We have found that inhibition of the complement cascade in vivo blocks fetal loss and growth restriction associated aPL antibodies. We have identified complement component C5, and particularly its cleavage product C5a, as key mediators of fetal loss. Ongoing studies are examining the initiators, inflammatory mediators, and the cellular effectors of aPL-induced fetal injury. Identification of complement components and downstream effectors that trigger aPL-associated injury will provide the basis for new therapies to improve outcomes in pregnant women with APS and, potentially, in pregnancy loss due to other immune mechanisms.

To translate our novel basic research observations on the role of complement in aPL-mediated pregnancy loss to patients, we have begun a prospective observational study. The goals of our study are:

• To determine whether there is a unique pattern of complement activation in patients with aPL-associated fetal loss.
  
• To generate substantial and convincing clinical data to launch a clinical trial of complement inhibitors for aPL-associated recurrent fetal loss.

We are recruiting over 400 pregnant patients, enrolled at 6 major clinical centers, and grouped and analyzed according to the presence or absence of aPL and preexisting SLE. We will obtain detailed medical and obstetrical information during the course of their pregnancies, serial blood specimens for complement and cytokine assays, and RNA to elucidate temporal changes in gene expression during the course of complicated and uncomplicated pregnancies. These data will be analyzed to identify predictors of poor fetal outcome. Characterization of clinically applicable surrogate markers that predict pregnancy complications will enable us to initiate an interventional trial of complement inhibition in patients at risk for aPL antibody-associated fetal loss. The identification of such surrogate markers in aPL and SLE patients may also prove generally applicable to anticipate complications during pregnancy in disease-free women.

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 (carotid plaque assessed by 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. These may define two disease patterns: one smoldering, prolonged disease that is accompanied by high damage score, limited production of autoantibodies confers vascular damage (atherosclerosis), and a second with more extensive autoimmunity and aggressive disease, often requiring cytotoxic therapy. 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 will test this hypothesis and examine the mechanisms of accelerated atheroscelerosis in patients with SLE and other autoimmune diseases.

The Role of Receptors for Immunoglobulin G in Autoimmune Diseases

FcgR are receptors on the surface of cells that bind the Fc portion of immunoglobulin G, thereby linking the humoral and cellular components of the immune system. Several critical observations by this laboratory have underscored the importance of FcgR to host defense and the pathogenesis of inflammatory disease.

• FcgR-dependent mononuclear phagocyte function is abnormal in human immune complex disease;
  
• Inherited variants of FcgR structure strongly influence receptor function: alleles of FcgRIIA and FcgRIIIA alter the ability of the receptors to bind human IgG and impact the risk of renal disease in SLE and of serious bacterial infection;
  
• FcgR alleles are abnormally distributed in human autoimmune diseases. The overall goals of ongoing studies are to understand structure-function relationships among FcgR and to further define the role of FcgR in the pathogenesis of autoantibody-mediated diseases.

Laboratory Personnel:

• Visiting Senior Scientist:
  Gloria Koo, PhD
  
  
• Postdoctoral Research Fellows:
  Xiaoping Qing, MD, PhD
  Shari Gelber, MD, PhD
  Danieli Andrade, MD
  Milena Vukelic, MD
  Diana Goldenberg, MD, MPH
  
• Research Associates:
  Marta Guerra, BS
  Patricia Redecha, BS
  Randi Eisner, MSW
  Michelle Perna, BA
  Laarni Quimson, BA
  Joan Rho, BA
  Emily Miller, BA

Research Interests

Systemic Lupus Erythematosus
Antiphospholipid Syndrome
Pregnancy in Autoimmune Patients
Cardiovascular Disease in Autoimmune Patients

Clinical Trials

• PROMISSE: Predictors of Pregnancy Outcome: Biomarkers in Anti-Phospholipid Antibody Syndrome (APS) and Systemic Lupus Erythematosus (SLE)
• Fc Receptor Function in Normals and Systemic Lupus Erythematosus (SLE)
• Autoimmune Disease Registry and Repository
• Scleroderma Registry