4 year PhD programme MRC-funded "From Bench to Bedside" studentships ON HOLD
This programme of study has been developed to offer students the unique opportunity to combine research training in cutting edge biomedical science and to experience the clinical context of the research.
1st Year (start: 2011)
2nd Year (start: 2010)
3rd Year (start: 2009)
(Click on highlighted names to read student experience)
I joined Dr. Clare Jolly’s research team in the Division of Infection and Immunity after two interesting and fruitful rotations: one in Dr. Mahdad Noursadeghi’s laboratory and another working with Dr. Ariberto Fassati. Our group is broadly interested in identifying cellular factors (and pathways) that regulate HIV-1 assembly in, and dissemination between, CD4 T cells - the main targets for HIV-1 infection in vivo. My work focuses on identifying determinants of HIV-1 cell-to-cell spread at virological synapses (VS). In particular, I wish to investigate:
Is there a functional role for microtubule organising centre polarisation to the VS?
Is there signalling at the VS which can contribute to efficient cell-to-cell spread of HIV-1?
Answering these questions will lead to a better understanding of viral pathogenesis and could potentially aid the search for new therapeutic interventions or vaccine design.
The rotational period of this scheme is an
extremely useful tool for enabling students to decide on a research group where
they will flourish. This, along with the opportunity to take an extremely wide
variety of courses offered by the graduate school, is one of the main strengths
of the Bench-to-Bedside PhD programme.
Before joining Prof. Arne Akbar’s group for my PhD, I rotated in Dr. David Escor’s lab to learn the basis of recombinant DNA technology, and its application to lentivector engineering. After, I decided to combine these lessons with my previous background regarding molecular mechanisms at the basis of T cell senescence. The main core of my PhD aims at setting up a lentivector-based strategy, under Prof. Akbar and Dr. Escor’s supervision, to reverse T cell senescence and re-establish telomerase activity in highly differentiated T lymphocytes. Furthermore, I am investigating the molecular bases of IFN- alpha mediated modulation of telomerase activity in CD8+ and CD4+ T lymphocytes. The molecular tuning of telomerase activity by a variety of ways may be applied to face several modern molecular medicine’s challenges, including cancer immunotherapy, autoimmune diseases and chronic viral infections. Finally, the possibility to shape our CV in the most suitable way, ensured by the flexibility of the scheme, is one of the most attractive points of strength of this MRC-funded B2B PhD program.
Upon joining the Bench to Bedside programme I undertook two very enjoyable (and insightful) rotations in the Virology department (Prof. Emery and Dr.Milne) and the Immunology department (Prof. Stauss) at the Royal Free Hospital before settling into my PhD in Prof. Mala Maini’s group. Our group focuses on the immunopathogenesis of chronic hepatitis B infection; recently the group have demonstrated that in infected patients who are unable to control the virus the immune system is disabled by progressive CD8 T exhaustion. My research is to focus on two key areas described below:
1) Dissecting how the nutrient microenvironment at the site of HBV infection influences T cell exhaustion. In previous work it has been highlighted that the depletion of the amino acid L-arginine may play a potential role in impairing T cell receptor signalling and function, so I aim to investigate the L-arginine depletion further and to look at the role of other nutrients that may also be dysregulated.
2) To consider a role for T cell senescence (as opposed to exhaustion) within the T cell population. Again preliminary data point towards a role for telomere-dependent and telomere-independent senescence (mediated by p38MAPK signalling) in highly differentiated T cells, that I will be following up on in the setting of chronic HBV.
I believe the strengths of the programme include not only the ability to experience different labs to see how they are run, the work carried out and a chance to determine whether this suits you, but also gives you the chance to acquire a diverse skill set, increase your own knowledge by attending taught courses and a great chance to translate basic research into the clinical environment.
My research examines how Neisseria meningitidis serogroup B (meningococcus) affects the cells of the immune system. Specifically, I am investigating how the bacterium can suppress the immunological function of human dendritic cells, which are crucial for generating a robust adaptive immune response. So far I have found that the bacteria can block the cellular signalling activity of potent immune stimulants (TLR agonists), possibly by interfering with a crucial molecular pathway. I have also found that the bacteria can actively polarise the T cell response which is generated by dendritic cells.
Meningococcus is the leading cause of childhood meningitis and septicaemia in the UK. Basic scientific research is needed to fully elucidate how this pathogen interacts with the immune system, and thereby develop vaccines and treatments to combat clinical disease.
One of the biggest strengths of the PhD programme is the rotational element in the first year. It allows students to discover which immunological themes they find the most interesting on a first-hand basis. Moreover, it means students acquire a diverse set of scientific skills from various UCL groups to bring to their chosen projects.
started my PhD at UCL in September of 2009, and did 3 rotations; 2 in HIV
research at the (now defunct) Windeyer building, and one in microbiology at the
Institute of Child Health. Despite initially looking for a virology project, I
realised I had become far more interested in the bacterial disease that I was
working on here. This, plus the friendly and relaxed atmosphere, won me over
and I chose to join the team of Garth Dixon and Nigel Klein in studying Neisseria
I study the role of E-selectin in meningococcal sepsis, E-selectin is essential in the recruitment of neutrophils and other immune cells to a site of infection, and is over-expressed in the blood vessels of children with meningococcal septicaemia. This can lead to immune complex formation in blood vessels and systemic shock. By studying expression patterns of E-selectin on endothelial cells we hope to discover new relationships and pathways involved in both infected and healthy bodies.
Page last modified on 16 oct 14 10:24