Chrissy Roberts PhD

Research Fellow

I graduated from University College London in 2001 with a B.Sc. in Biology; after which I joined the staff at the Anthony Nolan Research Institute (ANRI), where I worked as a research assistant to the European Searchable Tumour Cell Lines Database (ESTDAB) project. In 2004 I registered for a Ph.D. at the UCL Cancer Institute, based in the HLA informatics group at the ANRI. I came to the London School of Hygiene and Tropical Medicine in July 2008, where I work as a research fellow in the Department of Clinical Research as a member of the trachoma group.

Affiliation

Teaching

I am a tutor on the distance learning (DL) programme (ID-102 Principles of Biology). I am currently developing a new module "Reseach Methods for the Laboratory" that aims to teach practical skills in infectious disease research by distance learning. DL students may currently miss out on opportunities to obtain practical and laboratory based research experience as an integral part of their master's courses. I am interested in the use of new media, mobile technology, games, music and similar interactive content as tools to facilitate experiential distance learning.

Research

I am investigating a potential association between polymorphisms in immune response genes and the blinding sequelae of trachoma in the Gambian population. A disease of poverty, trachoma is characterised by scarring to the conjunctiva of the eye, which leads to a turning in of the eyelid and the resultant abrasion of the cornea by inward facing eye lashes. This leads to corneal opacity and eventual blindness. Trachoma is caused by the ocular serovars of Chlamydia trachomatis, an organism which is better known for its role in sexually transmitted disease.

Susceptibility to trachoma has been shown to depend largely upon a number of environmental risk factors and current control strategies aim in part to minimise exposure to these risks. Families who live together are likely to experience similar exposures to environmetnal risk factors for trachoma and we might assume that given a shared 'high risk' environment, all family members would develop the disease. This is clearly not the case and within families we see that some individuals develop severe phenotypes, whilst others may remain entirely unaffected or else affected, but to a lesser degree. This situation suggests the presence of one or more genetic factors that are randomly assorting through families and conferring protection from or susceptibility to trachomatous disease. We have estimated that nearly one third of the total risk of trachomatous scarring is attributable to genetic effects.

Our current study aims to identify immune response genes that contribute to the genetic attributable fraction of trachomatous scarring. In order to maximise our power to detect genetic risk factors, we have selected a population of Gambian families in which very young children have already developed trachomatous scarring. These families represent a population in which there is an extreme phenotype because scarring usually develops in later life. Young children have also had a lesser degree of exposure to environmental risk factors, so the scarring phenotype that develops in early childhood is likelier to be more readily attributable to genetic factors.

I am studying in detail the immunogenetic diversity of this population of families, with a focus on immunopolymorphisms relating to natural (innate) immunity and particularly on the genes which encode the cell surface receptors of Natural Killer (NK) cells. I am presently investigating how two families of immunoreceptors may associate with early onset scarring. These families, the Killer-cell Immunoglobulin-like Receptors (KIR) and the Human Leucocyte Antigen (HLA) complex, are known to interact with one another and complex combinations of polymorphisms in these gene systems have been shown to be associated with many phenotypes. Epistasis (gene-gene interaction) between KIR and HLA is known to affect differential outcomes of infectious and autoimmune diseases, of haematopoietic stem cell transplantation and of the risks of pre-eclampsia, spontaneous miscarriage and extremely high or low birth-weights.

In tandem with the association study, the family structure allows powerful analysis of the population genetics of the KIR gene system. The KIR complex is as highly complicated in its structure as it is in its function and much is unknown about the gene organisation and haplotype structures, particularly as most individuals do not carry a full complement of KIR genes on any given haplotype (KIR exhibits genotypic diversity). My aim is to determine the genotypic and haplotypic diversity of the Gambian families through a combination of segregation analysis and maximum likelihood methods. This will be the first large scale study to assess KIR diversity in an African population.

Other focus-points of my research include the development of novel methods to identify previously uncharacterised polymorphism in complex gene systems and also the development of new diagnostic assays for use in infectious disease research.

Research areas

  • Diagnostics
  • Human genetics
  • Innate immunity

Disciplines

  • Genetics
  • Immunology
  • Molecular biology

Disease and Health Conditions

  • Eye diseases
  • Infectious disease
  • Trachoma

Other interests

  • HLA
  • Immunogenetics
  • KIR
Back to top