Gail A. Bishop | |
---|---|
Alma mater | University of Wisconsin–Madison (BSc) University of Michigan (PhD) |
Awards | Elected Fellow of the American Association for the Advancement of Science |
Scientific career | |
Institutions | University of North Carolina at Chapel Hill University of Iowa |
Gail A. Bishop is an American professor of microbiology and immunology at the University of Iowa and director of the Center for Immunology & Immune-Based Diseases at the Carver College of Medicine.
Bishop was born in Wisconsin, United States. [1] She became interested in science as a teenager after first studying biology in the 9th grade. [1] She completed a summer job in a leukemia research laboratory in Milwaukee. [1] Bishop studied biology at St. Olaf College. [2] She earned a master's degree in oncology at the University of Wisconsin–Madison. Bishop moved to University of Michigan as a graduate student, working in cellular biology with Joseph Glorioso. Her doctoral degree involved research into the Herpes simplex virus. After completing her PhD Bishop was appointed as a postdoctoral fellow to the University of North Carolina at Chapel Hill where she worked on the mechanism of B lymphocyte activation and the structure-function relationships within B cell signalling receptors.
In 1989 Bishop was appointed as an assistant professor at the University of Iowa. She was promoted to professor in 1998, and in 2001 became the Distinguished Professor of Microbiology.
Bishop studies the molecular mechanisms that underlie lymphocyte regulation and activation by members of the TNF receptor superfamily. [3] [4] She studies lymphocyte signalling and the interaction between immune receptors. Her work involves studying the mechanisms by which the protein-coding gene TRAF3 deficiency regulates survival in B lymphocytes. She has shown that TRAF3 is a regulator of critical negative regulator of homeostatic survival in B lymphocytes. Through this research Bishop hopes to design new treatments for B lymphocyte malignancies.
She has also investigated the role of TRAF3 in T cell signalling and function, as well as trying to establish the nuclear roles of TRAF3. T cells that are deficient in TRAF3 have no clear differences in survival, but do have decreases in CD4+ and CD8+ responses to infection or immunisation. [1] Bishop showed that in T cells TRAF3 associates with the T-cell receptor (TCR) complex, which governs TCR-mediated activation.
Bishop believes that B lymphocytes could be used for immunotherapeutic cancer treatment, whereby B-cells can injected, become activated in vitro and serve as antigen-presenting cells. [2] B cell immunotherapy presents a promising alternative to using dendritic cells.
Alongside her scientific research, Bishop has spoken about the environment for women and other minoritized groups within academic science. [5]
Her awards and honours include:
Her publications include:
A T cell is a type of lymphocyte. T cells are one of the important white blood cells of the immune system and play a central role in the adaptive immune response. T cells can be distinguished from other lymphocytes by the presence of a T-cell receptor (TCR) on their cell surface.
B cells, also known as B lymphocytes, are a type of white blood cell of the lymphocyte subtype. They function in the humoral immunity component of the adaptive immune system. B cells produce antibody molecules; however, these antibodies are not secreted. Rather, they are inserted into the plasma membrane where they serve as a part of B-cell receptors. When a naïve or memory B cell is activated by an antigen, it proliferates and differentiates into an antibody-secreting effector cell, known as a plasmablast or plasma cell. Additionally, B cells present antigens and secrete cytokines. In mammals, B cells mature in the bone marrow, which is at the core of most bones. In birds, B cells mature in the bursa of Fabricius, a lymphoid organ where they were first discovered by Chang and Glick, which is why the 'B' stands for bursa and not bone marrow as commonly believed.
A cytotoxic T cell (also known as TC, cytotoxic T lymphocyte, CTL, T-killer cell, cytolytic T cell, CD8+ T-cell or killer T cell) is a T lymphocyte (a type of white blood cell) that kills cancer cells, cells that are infected by intracellular pathogens (such as viruses or bacteria), or cells that are damaged in other ways.
The adaptive immune system, also known as the acquired immune system, is a subsystem of the immune system that is composed of specialized, systemic cells and processes that eliminate pathogens or prevent their growth. The acquired immune system is one of the two main immunity strategies found in vertebrates.
The T-cell receptor (TCR) is a protein complex found on the surface of T cells, or T lymphocytes, that is responsible for recognizing fragments of antigen as peptides bound to major histocompatibility complex (MHC) molecules. The binding between TCR and antigen peptides is of relatively low affinity and is degenerate: that is, many TCRs recognize the same antigen peptide and many antigen peptides are recognized by the same TCR.
CD3 is a protein complex and T cell co-receptor that is involved in activating both the cytotoxic T cell and T helper cells. It is composed of four distinct chains. In mammals, the complex contains a CD3γ chain, a CD3δ chain, and two CD3ε chains. These chains associate with the T-cell receptor (TCR) and the CD3-zeta (ζ-chain) to generate an activation signal in T lymphocytes. The TCR, CD3-zeta, and the other CD3 molecules together constitute the TCR complex.
ZAP-70 is a protein normally expressed near the surface membrane of lymphocytes. It is most prominently known to be recruited upon antigen binding to the T cell receptor (TCR), and it plays a critical role in T cell signaling.
Tumor necrosis factor receptor superfamily, member 4 (TNFRSF4), also known as CD134 and OX40 receptor, is a member of the TNFR-superfamily of receptors which is not constitutively expressed on resting naïve T cells, unlike CD28. OX40 is a secondary co-stimulatory immune checkpoint molecule, expressed after 24 to 72 hours following activation; its ligand, OX40L, is also not expressed on resting antigen presenting cells, but is following their activation. Expression of OX40 is dependent on full activation of the T cell; without CD28, expression of OX40 is delayed and of fourfold lower levels.
CD137 is a member of the tumor necrosis factor (TNF) receptor family. Its alternative names are tumor necrosis factor receptor superfamily member 9 (TNFRSF9), 4-1BB and induced by lymphocyte activation (ILA). It is of interest to immunologists as a co-stimulatory immune checkpoint molecule.
CD27 is a member of the tumor necrosis factor receptor superfamily. It is currently of interest to immunologists as a co-stimulatory immune checkpoint molecule, and is the target of an anti-cancer drug in clinical trials.
Philippa "Pippa" Marrack, Ph.D, FRS is an English immunologist and academic, based in the United States, best known for her research and discoveries pertaining to T cells. Marrack is the Ida and Cecil Green Professor and chair of the Department of Biomedical Research at National Jewish Health and a Distinguished Professor of immunology and microbiology at the University of Colorado Denver.
Lymphocyte-activation gene 3, also known as LAG-3, is a protein which in humans is encoded by the LAG3 gene. LAG3, which was discovered in 1990 and was designated CD223 after the Seventh Human Leucocyte Differentiation Antigen Workshop in 2000, is a cell surface molecule with diverse biologic effects on T cell function. It is an immune checkpoint receptor and as such is the target of various drug development programs by pharmaceutical companies seeking to develop new treatments for cancer and autoimmune disorders. In soluble form it is also being developed as a cancer drug in its own right.
Harald von Boehmer was a German-Swiss immunologist best known for his work on T lymphocytes.
Christopher Edward Rudd, is a Canadian-born immunologist-biochemist. He is currently Professor of Medicine at the Universite de Montreal and Director, Immunology-Oncology at the Centre de Recherche Hôpital Maisonneuve-Rosemont (CR-HMR).
Frederick "Fred" W. Alt is an American geneticist. He is a member of the Immunology section of the National Academy of Sciences and a Charles A. Janeway Professor of Pediatrics, and Professor of Genetics at Harvard Medical School. He is the Director of the Program in Cellular and Molecular Medicine at the Boston Children's Hospital. He is a Howard Hughes Medical Institute investigator, since 1987.
Max Dale Cooper, ForMemRS, is an American immunologist and Professor of Pathology at Emory University known for identifying T cells and B cells.
Tasuku Honjo is a Japanese physician-scientist and immunologist. He won the 2018 Nobel Prize in Physiology or Medicine and is best known for his identification of programmed cell death protein 1 (PD-1). He is also known for his molecular identification of cytokines: IL-4 and IL-5, as well as the discovery of activation-induced cytidine deaminase (AID) that is essential for class switch recombination and somatic hypermutation.
Jean Sylvia Marshall, born in Birmingham, England, is a Canadian immunologist and acting Professor and Head of the Department of Microbiology & Immunology at Dalhousie University in Halifax, Nova Scotia, Canada. Marshall's work has investigated how mast cells are involved in the early immune response to infection and antigen. She is best known for her discovery of the previously unknown degranulation-independent immunoregulatory roles of mast cells in infection and allergy and their ability to mobilize dendritic cells.
Garnett Herrel Kelsoe is an American immunologist and the James B. Duke Professor of Immunology at Duke University School of Medicine.
Leslie Joan Berg is an American immunologist. As a professor at University of Massachusetts Medical School, she was elected the 95th president of the American Association of Immunologists for a one-year term from 2011 to 2012. Berg’s research focuses on understanding the signal transduction pathways—the succession of reactions inside the cell as it changes one kind of stimulus, or signal, into another—important for T-cell development and activation, and the generation of protective immunity to infections.
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