Immunology, Infection & Inflammatory Disease (IIID) (Research Division)

PhD

In London

£ 5,300 VAT inc.

Description

  • Type

    PhD

  • Location

    London

  • Duration

    3 Years

  • Start date

    Different dates available

Parallels between cytokinesis and retroviral budding: a role for the ESCRT machinery. Science
CD4+CD25+Foxp3+ regulatory T cells induce alternative activation of human monocytes/macrophages. Proc Natl AcadSci USA
The structural basis of T cell autoimmunity. Nature Immunology
Innate sensing of HIV-1 assembly by Tetherin induces NF-kB proinflammatory responses. Cell Host and Microbe
Nr4a1-dependent Ly6C(low) monocyte monitor endothelial cells and orchestrate their disposal. Cell
A revised classification of monocyte, macrophage, and dendritic cell development and subsetting. Science & Annu Rev Immunology
A novel linkage between lymphoid stress-surveillance and atopy. Science.
Epidermal Dendritic Cells promote carcinogenesis via metabolism of environmental hydrocarbons. Science
Human MX2 is an interferon-induced post-entry inhibitor of HIV-1 infection. Nature
MEF2 is an in vivo immune-metabolic switch. Cell

Facilities

Location

Start date

London
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Start date

Different dates availableEnrolment now open

About this course

Bachelor's degree with 2:1 honours in a relevant subject.

A 2:2 degree may be considered only where applicants also offer a Master's of Science degree with Merit or above.

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Reviews

Subjects

  • Immunology
  • Infection
  • Surveillance
  • Mechanisms
  • Microbial determinants
  • HIV-AIDS virus
  • AIDS virus
  • Cell Division
  • Diabetes
  • Cells
  • Monocyte
  • HIV pathogenesis
  • Cell-autonomous

Course programme

Description

Our Division uses a range of techniques from molecular genetics and biochemistry to clinical trial design to better understand the dynamic interplay between host defence mechanisms and viral and microbial determinants. These studies have exposed novel determinants of host protection against HIV-AIDS virus, and revealed how the virus depends upon key components of cell biology such as those that direct cell division. We examine what fails when host defence mechanisms mistakenly target uninfected tissues, causing autoimmune diseases such as rheumatoid arthritis and Type I Diabetes, and ask how such mechanisms respond to tumours.

One major focus is on a refined understanding of the function and turnover of monocytes; another on the characterization of a novel lymphoid stress-surveillance response; a third on the recognition of microbial infection; and a fourth on the nature of T cell dysregulation that underpins MHC-restricted autoimmune diseases. We actively consider practical approaches to enhancing host responses to pathogens and to limiting autoimmunity, and we contribute to clinical trials novel approaches to measuring disease course and treatment outcome.

Major research programmes include:

The study of lymphoid stress-surveillance in tumour rejection and in graft rejection; the mechanisms of action of human regulatory T cells; T cell development in the thymus; Factors that regulate the threshold for lymphocyte responses; Monocyte and dendritic cell function and development; The maturation of B cell responses in tissues; Approaches to immunotherapy; RNA trafficking and metabolism and its roles as in host defense and HIV pathogenesis; Viral budding mechanisms; Innate, cell-autonomous anti-viral responses and pattern recognition; Antigen non-specific activation of innate immunity; Leukocyte trafficking; B cell and T cell responses that operate at the body's surfaces; Vaccine and adjuvant design for both immunoprotection (infection / tumours); Immunosuppression (autoimmune disease); Hospital acquired infections and multi-centre clinical trialsViral vectors and genetic therapies.

We actively contribute to the Biomedical Research Centre of Guy’s and St Thomas’ Hospital Trusts, in which regard research into practical cell therapy programmes have just commenced.

We also have links with large and small pharmaceutical and biotech activities, via sponsored research agreements with Genentech, NovoNordisk, GSK, and ImmuoQure.

Course study environment

The Division currently has 45 PhD students each working on individual projects, within established teams of researchers, supervised by the Principal Investigator of the group and commonly interacting with fellow laboratory researchers on a day-today basis. Students are expected to submit their thesis within four years of the start of their studies - to achieve this they will need to work and think carefully and intensively on a daily basis. Departments run laboratory meetings, which students will be required to attend and there is a strong ethos of continued education, so students are encouraged to broaden their scientific knowledge by attending seminars in other departments within the Division. Students are supported throughout their three-year (FT) or six-year (PT) studies by a personal committee composed of the student's two Supervisors, two independent experts and a Chairperson, who is part of the Postgraduate Teaching Committee. The student has regular six-monthly reports/meetings to monitor progress. In addition, they present their work at laboratory and departmental meetings and at the annual divisional Graduate Students' Research Day.

Postgraduate training

Excellent training courses (scientific, IT and others) are available for all PhD students through King's Graduate School. Additionally, training for most laboratory techniques is available within the Division. It is expected that graduate students will attend many of these courses to help them rapidly attain the high level of technical and IT expertise required to produce top quality work.

Additional information

Part time tuition fees: £2,650 per year (MPhil/PhD)
                                    £2,650 per year (MPhil/PhD Clinical)
                                    £2,650 per year (MDRes)
                                    £2,650 per year (MDRes Clinical)

Immunology, Infection & Inflammatory Disease (IIID) (Research Division)

£ 5,300 VAT inc.