Charlotte Cunningham-Rundles, MD, PhD
- PROFESSOR | Medicine, Clinical Immunology
- PROFESSOR | Pediatrics
Specialty:Allergy and Immunology
Research Topics:Allergy, Apoptosis/Cell Death, Autoimmunity, B Cells, Biodefense, Cellular Differentiation, Dendritic Cells, Immunology, Mucosal Immunology
Dr. Cunningham-Rundles is the David S. Gottesman Professor of Immunology at the Mount Sinai School of Medicine in New York. She is a Professor of Medicine and Pediatrics, a member of the Immunology institute, and directs the Immunodeficiency Clinic at Mount Sinai. She is also the Program Director of the Allergy Immunology Fellowship training program. She received her MD from Columbia College of Physicians and Surgeons, and her PhD from New York University School of Medicine. Dr. Cunningham-Rundles is an expert in the more than 150 Primary Immune Deficiency diseases, conditions that result from genetic defects of the immune system. Her research has been supported by US Public Health Service, the Food and Drug Administration, and the National Institutes of Health (NIH) Division of Allergy Immunology and Transplantation.
Her contributions have been widely recognized, notably the Clinical Immunology Society President's Award, the Boyle Award Immune Deficiency Foundation award, the Abbott Award from the American Society for Microbiology, and the American Academy Asthma, Allergy, and Immunology Research Award where she has been on the Board of Directors. She is a Past President of the Clinical Immunology Society. Dr. Cunningham-Rundles has served as Chair of Allergy Immunology and Transplantation Committee for the National Institutes of Health and has Chaired the Immunology Review Committee of the National Aeronautics and Space Administration. She served on the Medical Advisory Boards of the Immune Deficiency Foundation, and the Jeffrey Modell Foundation. Dr. Cunningham-Rundles has served on the FDA Blood Safety and Advisory Committee and is the principal investigator of the USIDNET, a research cooperative sponsored by the NIH. She is a member of the International Union of Immunology Sciences Expert Committee on Immune Deficiency.
In the News
Dr. Cunningham-Rundles discusses immune deficiency disorders in The Daily News feature The Daily Check Up.
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American Board of Internal Medicine
- Fungal Infections
- Immune Deficiency (non-HIV)
Multi-Disciplinary Training AreaImmunology [IMM]
MD, Columbia University
PhD, New York University
Residency, Internal Medicine, Bellevue Hospital Center
Human immunodeficiency diseases; mechanisms and treatments
In this laboratory, the area of investigation is human immunodeficiency diseases and immuno-reconstitution. This work has been supported by research grants from the Food and Drug Administration and the NIH, Division of Allergy Immunology and Transplantation, Child Health and Human Development and USIDNet. We are investigating B, T cell and dendritic cell immunity in a primary immunodeficiency disease, common variable immunodeficiency (CVID.) A recent theme is the investigation of B cell memory in this and other immune defects; CD27+B cells, and especially isotype switched B memory cells are deficient, which is related to lack of normal vaccine responses. How the development of B cell memory relies upon triggering of Toll like Receptors is under investigation, using methylated oligonucleotides containing CpG motifs. TLR9 function is abnormal in this immune defect a factor that leads to poor B cell proliferation, loss of cytokine production, lack of cell adhesion and defective B cell memory responses; plasmacytoid dendritic cells are also unable to respond normally to these or other TLR ligands. We are also particularly interested in the role of specific mutations in the TACI gene, either producing or influencing the CVID phenotype, and the role of related TNF family members in the abnormal immunity in B cell defects. Further studies using gene arrays in the investigation of human B cell defects are ongoing. While the phenotype of this disease is hypogammaglobulinemia, T cell and antigen processing defects result in anergy, defective co-stimulation, accelerated apoptosis and deficient cytokine production. We previously found that some of these T cell defects could be reversed by the administration of IL-2, allowing an opportunity to explore some of the mechanisms by which this cytokine activates and regulates human T cell immunity. Since T cell receptor co-stimulation is abnormal in CVID, a deficiency of intracellular signaling pathways could explain defective proliferation, anergy, cytokine deficiency, and premature apoptosis. We have investigated in what way the CD28 signaling other co stimulatory pathways differ from normal T cells, analyzing early signaling events, membrane reorganization, up-regulation of Bcl-xL, and the effects of receptor triggering on transcription and stabilization of cytokine mRNA. In other studies we have found markedly deficient production of IL-12 by monocycle derived dendritic cells, a deficit that could further lead to anergy. We have also investigated ICOS gene and its ligand, in CVID subjects, since mutation of ICOS in humans can lead to the CVID phenotype.