REMINDER: Department of Infection, Immunity & Cardiovascular Disease Seminar – Monday 15th January 2018

Title: “PI3K in Immunity, Infection and Cancer”
Speaker: Professor Klaus Okkenhaug, University of Cambridge.
Venue: Lecture Theatre 3, F Floor Medical School.
Time: 12:30pm – 1:30pm
Abstract: The PI3K signalling pathway control many aspects of immune responses. The PI3Kδ isoform is selectively expressed cells of the immune system. Loss of PI3Kδ activity leads to impaired humoral immunity. However, loss of PI3Kδ in regulatory T cells can also contribute to enhanced immune responses, especially against cancer cells. Activated PI3Kδ syndrome is a primary immunodeficiency caused by mutations that lead to increased PI3Kδ activity. The fact that both loss of function and gain of function of PI3Kδ leads to immunodeficiency highlights how signalling pathways need to be dynamically regulated for normal immune cell function. Hyperactivity of PI3Kδ also leads to B cell transformation. Idelalisib is a PI3Kδ inhibitor, which has been approved for the treatment of certain B cell cancers. I will describe our approach to explore the roles of both loss and gain of PI3Kδ function in immunity, infection and cancer and discuss how PI3Kδ inhibitors for additional indications.

For enquiries, please contact: iicd@sheffield.ac.uk


FUTURE DATES FOR THE DIARY:

Tuesday 30th January 2018
Title:  “Regulation of Autophagy flux: Implications in neurodegenerative and infectious diseases”
Speaker:  Professor Ravi Manjithaya, Jawaharlal Nehru Centre for Advanced Scientific Research.
Venue:  Lecture Theatre 3, F Floor Medical School.
Time:  12:30pm – 1:30pm
Abstract:  The conserved intracellular eukaryotic process of (macro) Autophagy plays a key role in maintaining cellular homeostasis. Autophagy can capture damaged, unwanted and superfluous cytosolic contents including organelles and deliver them to lysosomes for degradation and recycling. Impairment in this process is associated in wide ranging diseases such as neurodegeneration, intracellular infectious diseases and cancer. Although recent studies have taken enormous strides in understanding autophagy process, little is known about how the rate of autophagy flux is governed. Employing an indigenous high throughput assay, my lab has identified several small molecule modulators of autophagy flux. Mechanism of action of some these molecules have shed light on interesting modes of regulation of autophagy flux. Some of these potent molecules also have therapeutic implications in certain diseases associated with autophagy dysfunction. I will highlight some of these aspects during my talk.

Tuesday 20th February 2018
Title:  “Seek and modify: CRISPR-Cas gene editing in the mouse”
Speaker:  Professor Neil Dear, University of Leicester.
Venue:  Lecture Theatre 3, F Floor Medical School.
Time:  12:30pm – 1:30pm
Abstract:  The mouse has become the pre-eminent mammalian animal model used in biomedical research. One of the features that has led to its dominance is the relative ease with which its genome can be modified. CRISPR-Cas technology has made this even easier and more powerful, and I will describe some of the models produced for research groups using this new method, its advantages over previous technologies, and our future plans for generating even better biomedical research models.