Dmitry Gabrilovich | |
---|---|
Born | |
Occupation | Researcher, professor |
Years active | 1984–present |
Dmitry Gabrilovich is currently a Chief Scientist, Cancer Immunology at AstraZeneca in Gaithersburg, MD, USA. His research is focused on methods by which tumors are able to suppress the immune system and how to develop new immune therapies to combat this ability. Gabrilovich described the defective ability of dendritic cells in induce immune responses in cancer, and was one of the discoverers of myeloid-derived suppressor cells (MDSC). The Gabrilovich lab focuses on immature myeloid cell biology and its relation to cancer. MDSC have been linked to a number of signaling pathways associated with cancer, including NF-κB, Jak-STAT, Notch, Wnt, and Rb, among others. [1] [2] His research has found that tumor cells can go through a mechanism that produces a free radical peroxynitrite, causing them to become resistant to certain types of cancer immunotherapy. [3] His research has also focused on monocytic-myeloid derived suppressor cells and polymorphonuclear-myeloid derived suppressor cells and what impact they might have on cancer therapy, since myeloid derived suppressor cells negatively regulate anti-tumor activity. [4] His group described methods of targeting suppressive myeloid cell. In 2019 he was awarded title of Research Professor by American Cancer Society. [5] Prior to joining AstraZeneca, Gabrilovich was a researcher and Christopher M. Davis professor at The Wistar Institute in Philadelphia. [6] [7] Prior to joining The Wistar Institute, Gabrilovich was a senior member at the Moffitt Cancer Center in Tampa. [2]
Some of Gabrilovich's most-cited publications include:
Dendritic cells (DCs) are antigen-presenting cells of the mammalian immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems.
Cancer immunotherapy is the artificial 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 subspeciality of oncology.
An antigen-presenting cell (APC) or accessory cell is a cell that displays antigen bound by major histocompatibility complex (MHC) proteins on its surface; this process is known as antigen presentation. T cells may recognize these complexes using their T cell receptors (TCRs). APCs process antigens and present them to T-cells.
Cross-presentation is the ability of certain professional antigen-presenting cells (mostly dendritic cells) to take up, process and present extracellular antigens with MHC class I molecules to CD8 T cells (cytotoxic T cells). Cross-priming, the result of this process, describes the stimulation of naive cytotoxic CD8+ T cells into activated cytotoxic CD8+ T cells. This process is necessary for immunity against most tumors and against viruses that infect dendritic cells and sabotage their presentation of virus antigens. Cross presentation is also required for the induction of cytotoxic immunity by vaccination with protein antigens, for example, tumour vaccination.
CD16, also known as FcγRIII, is a cluster of differentiation molecule found on the surface of natural killer cells, neutrophils, monocytes, and macrophages. CD16 has been identified as Fc receptors FcγRIIIa (CD16a) and FcγRIIIb (CD16b), which participate in signal transduction. The most well-researched membrane receptor implicated in triggering lysis by NK cells, CD16 is a molecule of the immunoglobulin superfamily (IgSF) involved in antibody-dependent cellular cytotoxicity (ADCC). It can be used to isolate populations of specific immune cells through fluorescent-activated cell sorting (FACS) or magnetic-activated cell sorting, using antibodies directed towards CD16.
Antigenic escape occurs when the immune system of a host, especially of a human being, is unable to respond to an infectious agent, or in other words that the host's immune system is no longer able to recognize and eliminate a pathogen such as a virus. This process can occur in a number of different ways of both a genetic and an environmental nature. Such mechanisms include homologous recombination, and manipulation and resistance of the host's immune responses.
Cancer immunology is an interdisciplinary branch of biology that is concerned with understanding the role of the immune system in the progression and development of cancer; the most well known application is cancer immunotherapy, which utilises the immune system as a treatment for cancer. Cancer immunosurveillance and immunoediting are based on protection against development of tumors in animal systems and (ii) identification of targets for immune recognition of human cancer.
5′-nucleotidase (5′-NT), also known as ecto-5′-nucleotidase or CD73, is an enzyme that in humans is encoded by the NT5E gene. CD73 commonly serves to convert AMP to adenosine.
Nicholas P. Restifo is an American immunologist, physician and educator in cancer immunotherapy. Until July 2019, he was a tenured senior investigator in the intramural National Cancer Institute of the National Institutes of Health at Bethesda, Maryland.Nicholas is now the executive vice president of research at Lyell based in San Francisco.
Professor Gustav Gaudernack is a scientist working in the development of cancer vaccines and cancer immunotherapy. He has developed various strategies in immunological treatment of cancer. He is involved in several ongoing cellular and immuno-gene therapeutic clinical trials and his research group has put major efforts into the development of various T cell-based immunotherapeutic strategies.
Tumor-associated macrophages (TAMs) are a class of immune cells present in high numbers in the microenvironment of solid tumors. They are heavily involved in cancer-related inflammation. Macrophages are known to originate from bone marrow-derived blood monocytes or yolk sac progenitors, but the exact origin of TAMs in human tumors remains to be elucidated. The composition of monocyte-derived macrophages and tissue-resident macrophages in the tumor microenvironment depends on the tumor type, stage, size, and location, thus it has been proposed that TAM identity and heterogeneity is the outcome of interactions between tumor-derived, tissue-specific, and developmental signals.
The tumor microenvironment (TME) is the environment around a tumor, including the surrounding blood vessels, immune cells, fibroblasts, signaling molecules and the extracellular matrix (ECM). The tumor and the surrounding microenvironment are closely related and interact constantly. Tumors can influence the microenvironment by releasing extracellular signals, promoting tumor angiogenesis and inducing peripheral immune tolerance, while the immune cells in the microenvironment can affect the growth and evolution of cancerous cells.
Myeloid-derived suppressor cells (MDSC) are a heterogeneous group of immune cells from the myeloid lineage.
Immune checkpoints are regulators of the immune system. These pathways are crucial for self-tolerance, which prevents the immune system from attacking cells indiscriminately. However, some cancers can protect themselves from attack by stimulating immune checkpoint targets.
A pre-metastatic niche is an environment in a secondary organ that can be conducive to the metastasis of a primary tumor. Such a niche provides favorable conditions for growth, and eventual metastasis, in an otherwise foreign and hostile environment for the primary tumor cells. This concept demonstrated the fundamental role of the microenvironment in regulating tumor growth and metastasis. The discovery of the pre-metastatic niche has fostered new research regarding the potential treatment of metastases, including targeting myeloid derived suppressor cells/myeloid cells, and stromal cell plasticity including fibroblasts and pericytes and perivascular smooth muscle cells and (attempts to stop the flow of vesicles from primary tumors to pre-metastatic niches in secondary organs and different combinations of microenvironment targeted therapies.
Type 1 regulatory cells or Tr1 (TR1) cells are a class of regulatory T cells participating in peripheral immunity as a subsets of CD4+ T cells. Tr1 cells regulate tolerance towards antigens of any origin. Tr1 cells are self or non-self antigen specific and their key role is to induce and maintain peripheral tolerance and suppress tissue inflammation in autoimmunity and graft vs. host disease.
Dendritic cells (DCs) are powerful antigen presenting cells for the induction of antigen specific T cell response. DC vaccine has been introduced as a new therapeutic strategy in cancer patients. DC-based immunotherapy is safe and can promote antitumor immune responses and prolonged survival of cancer patients.
Mikael Pittet is a Swiss research scientist.
Jacques Banchereau is an internationally prominent French American immunologist and molecular biologist. As of 2018, he is professor and director of immunological sciences at the Jackson Laboratory for Genomic Medicine. He was also the former chief science officer, senior vice president, and DTA head of inflammation & virology at Hoffman-La Roche. He is best known for his extensive research on dendritic cells with Nobel Laureate Ralph M. Steinman. He is the fifth most cited immunologist ranked by Times Higher Education's report.
Miram Merad is an Algerian professor in Cancer immunology and the Director of the Precision Immunology Institute at the Icahn School of Medicine at Mount Sinai in New York City, NY. She is the corecipient of the 2018 William B. Coley Award for Distinguished Research in Basic Immunology and a member of the United States National Academy of Sciences.