Adrian Hayday

Immunosurveillance Laboratory

The group is focused on understanding how lymphocytes function within epithelial tissues.

We have developed the 'Lymphoid Stress Surveillance' hypothesis whereby tissue-associated T cells recognise and respond rapidly to perturbations to epithelia cells. This under-studied biology is distinguishable from conventional T cell responsiveness by its rapidity and by its capacity to monitor perturbations induced by non-microbial challenges, such as carcinogens or oxidative stress.

The implications are that tissue-associated T cells can identify and eradicate transformed cells early en route to malignancy.

Consistent with this, lymphoid stress-surveillance includes the engagement by T cells of specific molecules upregulated on epithelial cell surfaces as a result of epidermal growth factor receptor dysregulation, as often occurs in tumours. Indeed, the lack of tissue-associated T cells significantly increases susceptibility to chemical carcinogens. Moreover, tumours and many types of virus employ immuno-evasive strategies to disarm this pathway of surveillance. Ongoing efforts aim to define the full range of molecules and pathways - the lingua franca - by which epithelial cell dysregulation is communicated to T cells, and the functional consequences thereof.

In this regard, our most recent studies have identified a new family of genes, expressed primarily by epithelial cells, upon which the composition of tissue-associated T cell compartments depends. We are also investigating the immunotherapeutic potential of tissue-associated T cell transfusion to patients, research which is conducted by members of our laboratory based at the Guy's Hospital Campus of King's College London.

Tissues at steady-state can be replete with immune cells.

Tissues at steady-state can be replete with immune cells. Photomicrograph of murine epidermis showing Langerhans cells (LC) (blue), T cells (red) and T cells that are not contacting LC (yellow). Imaging (Definiens) allows us to screen for regulators of cell type, number, density, size, and shape.

Selected publications

Gibbons D, Fleming P, Virasami A, Michel ML, Sebire NJ, Costeloe K, Carr R, Klein N, Hayday A. Interleukin-8 (CXCL8) production is a signatory T cell effector function of human newborn infantsNature Medicine. 2014 Sep 21. doi: 10.1038/nm.3670.

Vantourout P, Willcox C, Turner A, Swanson CM, Haque Y, Sobolev O, Grigoriadis A, Tutt A, Hayday A. Immunological Visibility: Posttranscriptional Regulation of Human NKG2D Ligands by the EGF Receptor PathwayScience Translational Medicine. 2014;6(231):231ra49.

Wencker M, Turchinovich G, Di Marco Barro R, Deban L, Jandke A, Cope A, Hayday A.  Innate-like T cells straddle innate and adaptive immunity by revising antigen-receptor responsivenessNature Immunology. 2014:5(1):80-87

Strid, J., Sobolev, O., Zavirova, B., Polic, B., and Hayday, A.C. The intraepithelial T cell response to NKG2D-ligands links lymphoid stress- surveillance to atopyScience 2011:334:1293-1297

Turchinovich, G and Hayday A. Skint-1 identifies a common molecular mechanism for the selective differentiation of IFN-gamma and IL-17-secreting gamma delta T cellsImmunity 2011:22: 59-68

Adrian Hayday

adrian.hayday@crick.ac.uk
+44 (0) 20 7269 3293

  • Qualifications and history
  • 1979 PhD, Imperial College London, UK
  • 1982 Postdoctoral, MIT, USA
  • 1985 Faculty, Yale University, USA
  • 1998 King's College London School of Medicine, UK
  • 2009 Established lab at the London Research Institute, Cancer Research UK
  • 2015 Group Leader, the Francis Crick Institute, London, UK