Michel C. Nussenzweig | |
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Born | São Paulo, Brazil | February 10, 1955
Education |
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Alma mater | New York University (B.A., 1975) |
Spouse | Svetlana Mojsov |
Scientific career | |
Fields | Immunology Molecular Biology |
Institutions | The Rockefeller University |
Michel C. Nussenzweig (born February 10, 1955) is a professor and head of the Laboratory of Molecular Immunology at The Rockefeller University and a Howard Hughes Medical Institute investigator. He is a member of both the US National Academy of Medicine and the US National Academy of Sciences.
Nussenzweig graduated summa cum laude with a B.A. degree from New York University College of Arts and Sciences in 1975. He earned a Ph.D. from The Rockefeller University in 1981 in cellular immunology, working in Zanvil A. Cohn’s laboratory with Ralph M. Steinman on groundbreaking studies of mouse dendritic cells.
As a Ph.D. student, Nussenzweig was the first to show that dendritic cells present foreign antigens to initiate T cell immunity. [1] He also produced the first dendritic cell-specific monoclonal antibody and cloned the first dendritic cell receptor. [2]
Nussenzweig received an M.D. from New York University School of Medicine in 1982 and completed his internship and residency in internal medicine, and a clinical fellowship in infectious diseases at Massachusetts General Hospital in 1985. From 1986 to 1989, he was a postdoctoral fellow in genetics in the Harvard Medical School laboratory of Philip Leder. Nussenzweig returned to The Rockefeller University as an assistant professor in 1990 and he became an associate professor in 1994, and a professor and senior physician in 1996. In 2013, he was named the first Zanvil A. Cohn and Ralph M. Steinman Professor. [3] [4]
Nussenzweig studies molecular aspects of the immune system’s adaptive and innate responses, using a combination of biochemistry, molecular biology, and genetics. Work on adaptive immunity focuses on B lymphocytes and antibodies to HIV-1, while work on innate immunity focuses on dendritic cells. [5] The laboratory has isolated and cloned human antibodies to HIV-1 and explored their roles in prevention and therapy. In clinical trials, a broadly neutralizing antibody isolated from an HIV-infected patient was shown to be safe and effective and to interfere with chronic infection in a way that traditional antiretroviral therapy does not. [6] [7] His research has led to the development of innovative vaccines against infectious diseases and new treatments for autoimmunity. [8] [9]
A DNA vaccine is a type of vaccine that transfects a specific antigen-coding DNA sequence into the cells of an organism as a mechanism to induce an immune response.
A monoclonal antibody is an antibody produced from a cell lineage made by cloning a unique white blood cell. All subsequent antibodies derived this way trace back to a unique parent cell.
Cancer immunotherapy is the stimulation of the immune system to treat cancer, improving on the immune system's natural ability to fight the disease. It is an application of the fundamental research of cancer immunology and a growing subspecialty of oncology.
In molecular biology, CD4 is a glycoprotein that serves as a co-receptor for the T-cell receptor (TCR). CD4 is found on the surface of immune cells such as T helper cells, monocytes, macrophages, and dendritic cells. It was discovered in the late 1970s and was originally known as leu-3 and T4 before being named CD4 in 1984. In humans, the CD4 protein is encoded by the CD4 gene.
Antonio Lanzavecchia is an Italian and Swiss immunologist. As a fellow of Collegio Borromeo he obtained a degree with honors in Medicine in 1976 from the University of Pavia where he specialized in Pediatrics and Infectious Diseases. He is Head Human Immunology Program, Istituto Nazionale di Genetica Molecolare-INGM, Milan and SVP Senior research Fellow, Humabs/Vir Biotechnology, Bellinzona and San Francisco (USA). Since 2017, he is also Professor at the Faculty of Biomedical Sciences of the Università della Svizzera italiana (USI).
Antibody-dependent enhancement (ADE), sometimes less precisely called immune enhancement or disease enhancement, is a phenomenon in which binding of a virus to suboptimal antibodies enhances its entry into host cells, followed by its replication. The suboptimal antibodies can result from natural infection or from vaccination. ADE may cause enhanced respiratory disease, but is not limited to respiratory disease. It has been observed in HIV, RSV virus and Dengue virus and is monitored for in vaccine development.
CD4 immunoadhesin is a recombinant fusion protein consisting of a combination of CD4 and the fragment crystallizable region, similarly known as immunoglobulin. It belongs to the antibody (Ig) gene family. CD4 is a surface receptor for human immunodeficiency virus (HIV). The CD4 immunoadhesin molecular fusion allow the protein to possess key functions from each independent subunit. The CD4 specific properties include the gp120-binding and HIV-blocking capabilities. Properties specific to immunoglobulin are the long plasma half-life and Fc receptor binding. The properties of the protein means that it has potential to be used in AIDS therapy as of 2017. Specifically, CD4 immunoadhesin plays a role in antibody-dependent cell-mediated cytotoxicity (ADCC) towards HIV-infected cells. While natural anti-gp120 antibodies exhibit a response towards uninfected CD4-expressing cells that have a soluble gp120 bound to the CD4 on the cell surface, CD4 immunoadhesin, however, will not exhibit a response. One of the most relevant of these possibilities is its ability to cross the placenta.
Ralph Marvin Steinman was a Canadian physician and medical researcher at Rockefeller University, who in 1973 discovered and named dendritic cells while working as a postdoctoral fellow in the laboratory of Zanvil A. Cohn, also at Rockefeller University. Steinman was one of the recipients of the 2011 Nobel Prize in Physiology or Medicine.
Fc fragment of IgG receptor IIb is a low affinity inhibitory receptor for the Fc region of immunoglobulin gamma (IgG). FCGR2B participates in the phagocytosis of immune complexes and in the regulation of antibody production by B lymphocytes.
2F5 is a broadly neutralizing human monoclonal antibody (mAb) that has been shown to bind to and neutralize HIV-1 in vitro, making it a potential candidate for use in vaccine synthesis. 2F5 recognizes an epitope in the membrane-proximal external region (MPER) of HIV-1 gp41. 2F5 then binds to this epitope and its constant region interacts with the viral lipid membrane, which neutralizes the virus.
A neutralizing antibody (NAb) is an antibody that defends a cell from a pathogen or infectious particle by neutralizing any effect it has biologically. Neutralization renders the particle no longer infectious or pathogenic. Neutralizing antibodies are part of the humoral response of the adaptive immune system against viruses, intracellular bacteria and microbial toxin. By binding specifically to surface structures (antigen) on an infectious particle, neutralizing antibodies prevent the particle from interacting with its host cells it might infect and destroy.
Barton Ford Haynes is an American physician and immunologist internationally recognized for work in T-cell immunology, retrovirology, and HIV vaccine development. Haynes is a Frederic M. Hanes Professor of Medicine and Immunology at Duke University Medical Center. He is the director of the Duke Human Vaccine Institute and the Duke Center for HIV/AIDS Vaccine Immunology and Immunogen Discovery (CHAVI-ID), which was funded by the National Institute of Allergy and Infectious Diseases (NIAID) in 2012. In addition, Haynes directs the B-cell Lineage Envelope Design Study, the Centralized Envelope Phase I Study, and the Role of IgA in HIV-1 Protection Study as part of the Collaboration for AIDS Vaccine Discovery (CAVD), which was funded by the Bill and Melinda Gates Foundation in 2006.
Zanvil Alexander Cohn was a cell biologist and immunologist who upon his death was described by The New York Times as being "in the forefront of current studies of the body's defenses against infection.", professor at Rockefeller University. There Cohn had been the Henry G. Kunkel Professor for seven years. Cohn was senior physician at the university as well as vice president for medical affairs. Until two years before his death, he also served as principal investigator of the Irvington Institute for Medical Research. Although Cohn never won the Nobel Prize, Ralph M. Steinman, with whom he ran a laboratory at Rockefeller University for many years, was named to win the 2011 Nobel Prize in Physiology or Medicine for the work on dendritic cells done in their lab, eighteen years after Cohn's death.
Susan Zolla-Pazner is an American research scientist who is a Professor of Medicine in the Division of Infectious Diseases and the Department of Microbiology at Mount Sinai School of Medicine and a guest investigator in the Laboratory of Molecular Immunology at The Rockefeller University, both in New York City. Zolla-Pazner's work has focused on how the immune system responds to the human immunodeficiency virus (HIV) and, in particular, how antibodies against the viral envelope develop in the course of infection.
Intrastructural help (ISH) is where T and B cells cooperate to help or suppress an immune response gene. ISH has proven effective for the treatment of influenza, rabies related lyssavirus, hepatitis B, and the HIV virus. This process was used in 1979 to observe that T cells specific to the influenza virus could promote the stimulation of hemagglutinin specific B cells and elicit an effective humoral immune response. It was later applied to the lyssavirus and was shown to protect raccoons from lethal challenge. The ISH principle is especially beneficial because relatively invariable structural antigens can be used for the priming of T-cells to induce humoral immune response against variable surface antigens. Thus, the approach has also transferred well for the treatment of hepatitis B and HIV.
Marina Fernandes De Barros Caskey is a Brazilian Physician-scientist, immunologist and professor at Rockefeller University.
Nina Papavasiliou is an immunologist and Helmholtz Professor in the Division of Immune Diversity at the German Cancer Research Center in Heidelberg, Germany. She is also an adjunct professor at the Rockefeller University, where she was previously associate professor and head of the Laboratory of Lymphocyte Biology. She is best known for her work in the fields of DNA and RNA editing.
Gwendalyn J. Randolph is an American immunologist, the Emil R. Unanue Distinguished Professor in the Department of Immunology and Pathology at Washington University in St. Louis, Missouri, where she is currently co-director of the Immunology Graduate Program. During her postdoctoral work, Randolph characterized monocyte differentiation to dendritic cells and macrophages and made advances in our understanding of dendritic cell trafficking and the fate of monocytes recruited to sites of inflammation. Her lab has contributed to the Immunological Genome Project by characterizing macrophage gene expression. Her work now focuses on the immunological mechanisms driving atherosclerosis and inflammatory bowel disease (IBD) by exploring lymphatic function and lipoprotein trafficking.
John R. Mascola is an American physician-scientist, immunologist and infectious disease specialist. He was the director of the Vaccine Research Center (VRC), part of the National Institute of Allergy and Infectious Diseases (NIAID), National Institutes of Health (NIH). He also served as a principal advisor to Anthony Fauci, director of NIAID, on vaccines and biomedical research affairs. Mascola is the current Chief Scientific Officer for ModeX Therapeutics.
Oligoclonal antibodies are an emerging immunological treatment relying on the combinatory use of several monoclonal antibodies (mAb) in one single drug. The composition can be made of mAb targeting different epitopes of a same protein (homo-combination) or mAb targeting different proteins (hetero-combination). It mimicks the natural polyclonal humoral immunological response to get better efficiency of the treatment. This strategy is most efficient in infections and in cancer treatment as it allow to overcome acquired resistance by pathogens and the plasticity of cancers.